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bp(GO:memory)

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Entity

Name
memory
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 31

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

Proteolytic processing of Alzeimer's beta-amyloid precursor protein v1.0.1

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. v1.0.0

This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014

Nicotinic Acetylcholine Receptors and Nicotinic Cholinergic Mechanisms of the Central Nervous System v1.0.0

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

NACHO Mediates Nicotinic Acetylcholine Receptor Function throughout the Brain v1.0.0

Neural Systems Governed by Nicotinic Acetylcholine Receptors: Emerging Hypotheses v1.0.0

Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Imbalances in the Hsp90 Chaperone Machinery: Implications for Tauopathies v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

The role of inflammasome in Alzheimer’s disease v1.0.3

PP2A and Alzheimer Disease v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Tau in physiology and pathology v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome v1.0.0

The autism/neuroprotection-linked ADNP/NAP regulate the excitatory glutamatergic synapse v1.0.0

In-Edges 112

act(a(MESH:"Lymphatic Vessels")) increases bp(GO:memory) View Subject | View Object

Similar impairments in spatial learning and memory were observed in mice that had undergone lymphatic ligation (Extended Data Fig. 5g–j), supporting the notion that the observed effect is a result of dysfunctional meningeal lymphatic drainage and not an artefact of the ablation method using visudyne PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

act(a(MESH:"Lymphatic Vessels")) increases bp(GO:memory) View Subject | View Object

Significant transcriptional alterations were also associated with excitatory synaptic remodelling and plasticity, hippocampal neuronal transmission, learning and memory and ageing-related cognitive decline (Extended Data Fig. 5q, r) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

a(CHEBI:"amyloid fibril") causesNoChange bp(GO:memory) View Subject | View Object

It was also demonstrated that fibril-free AβO solutions are essential for memory loss (Brito-Moreira et al. 2017), while the fibrillar Aβ in amyloid deposits is not the active factor affecting the cognition (Martins et al. 2008). PubMed:29196815

Appears in Networks:
Annotations
Confidence
High

a(HBP:HBP00074) decreases bp(GO:memory) View Subject | View Object

It was also demonstrated that fibril-free AβO solutions are essential for memory loss (Brito-Moreira et al. 2017), while the fibrillar Aβ in amyloid deposits is not the active factor affecting the cognition (Martins et al. 2008). PubMed:29196815

Appears in Networks:
Annotations
Confidence
High

a(HBP:HBP00074) decreases bp(GO:memory) View Subject | View Object

It was also shown that soluble AβOs may directly trigger dysfunction of neural signaling, which leads to early memory loss and the progression of dementia in AD. PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

a(HBP:HBP00074) decreases bp(GO:memory) View Subject | View Object

In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

a(CHEBI:"amyloid-beta") decreases bp(GO:memory) View Subject | View Object

Although excessive Abeta causes synaptic dysfunction and synapse loss [142], low levels of Abeta increase hippocampal longterm potentiation and enhances memory, indicating a novel positive, modulatory role on neurotransmission and memory [158,159] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Endosomes
Confidence
High
MeSH
Neurons
MeSH
Down Syndrome

p(HGNC:BACE1) decreases bp(GO:memory) View Subject | View Object

BACE1 deficiency in AD model mice have been shown to rescue cholinergic dysfunction, neuronal loss and memory deficits, correlating with a dramatic reduction in Abeta40/42 levels [79-81] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Endosomes
Confidence
Medium
MeSH
Neurons

a(HBP:HBP00067) increases bp(GO:memory) View Subject | View Object

In vivo studies have also shown that sAPP-alpha promotes learning and memory in animal models (Meziane et al. 1998; Taylor et al. 2008) PubMed:22122372

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons

a(CHEBI:epibatidine) causesNoChange bp(GO:memory) View Subject | View Object

The loss of nAChR subunits, as determined by [3H]- epibatidine binding, seems to take place after the transition from mild cognitive impairment (MCI) to AD (Sabbagh et al., 2006), although the loss of epibatidine binding did not correlate with decline in memory, cognitive performance, or with the development of neurofibrillary tangles or plaques (Sabbagh et al., 2001). PubMed:19293145

Appears in Networks:

composite(p(HGNC:MAPK1), p(HGNC:MAPK3)) association bp(GO:memory) View Subject | View Object

Which pathway is activated by Abeta depends upon the time of exposure to the amyloid peptide: chronic applications of oligomeric Abeta to hippocampal slice cultures activate the JNK/MAPK pathway but inhibit the ERK/MAPK pathway, whereas short-term applications of Abeta oligomers do not activate JNK (Bell et al., 2004). This may be one of the routes whereby Abeta impairs memory, because ERK-1 and ERK-2 play key roles in the signaling events central to memory (Satoh et al., 2007). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Hippocampus

path(MESH:"Alzheimer Disease") decreases bp(GO:memory) View Subject | View Object

Alzheimer’s disease (AD) is the most common form of dementia in elderly persons. It is a neurodegenerative disease marked by decline in memory and cognitive performance, including deterioration of language as well as defects in visual and motor coordination, and eventual death (for review, see Cummings, 2004). PubMed:19293145

Appears in Networks:

a(MESH:"1-(4-methoxybenzyl)-4-oxo-1,4-dihydroquinoline-3-carboxylic acid") increases bp(GO:memory) View Subject | View Object

Additionally, recent studies demonstrated that BQCA was effective in reversing memory deficits in Y-maze object recognition and spontaneous alternation tasks in rats.71,72 PubMed:24511233

Appears in Networks:

a(MESH:"Cerebral Cortex") association bp(GO:memory) View Subject | View Object

The popular amyloid cascade hypothesis posits that the gradual build-up of Abeta plaques leads to neuronal inflammation, dysfunction, and, eventually, cell death. The two brain regions most critically affected by this degeneration are the cortex and hippocampus, both of which are involved in cognition, learning, and memory. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(MESH:"Cerebral Cortex") association bp(GO:memory) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(MESH:"Prefrontal Cortex") association bp(GO:memory) View Subject | View Object

In brain slice electrophysiology studies, BQCA enhanced excitatory postsynaptic currents in medial prefrontal cortical neurons,69 an area critical for higher cognitive, learning, and memory functions.70 In pre-clinical animal studies, BQCA reversed scopolamine-impaired contextual fear conditioning and rescued medial prefrontal cortex-dependent discrimination reversal learning deficits in a transgenic mouse model of AD. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Prefrontal Cortex

a(MESH:Hippocampus) association bp(GO:memory) View Subject | View Object

The popular amyloid cascade hypothesis posits that the gradual build-up of Abeta plaques leads to neuronal inflammation, dysfunction, and, eventually, cell death. The two brain regions most critically affected by this degeneration are the cortex and hippocampus, both of which are involved in cognition, learning, and memory. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(MESH:Hippocampus) association bp(GO:memory) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:"long-term synaptic potentiation") association bp(GO:memory) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

path(MESH:"Alzheimer Disease") association bp(GO:memory) View Subject | View Object

Conversely, the most commonly associated symptoms of AD are cognitive in nature and include deficits in learning and memory. However, 50%–80% of AD patients display psychotic and behavioral disturbances that are correlated with poor social and functional outcomes PubMed:24511233

Appears in Networks:

a(CHEBI:"dihydro-beta-erythroidine") decreases bp(GO:memory) View Subject | View Object

For example, local infusion of the α7 antagonist, methyllycaconitine (MLA), or the β2∗ antagonist, dihydro-β-erythroidine (DHβE), into the basolateral amygdala, the ventral hippocampus, or the dorsal hippocampus impairs the working memory of rats seeking food reward within a 16-arm radial maze (146–148). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
Hippocampus

a(CHEBI:"nicotinic acetylcholine receptor agonist") increases bp(GO:memory) View Subject | View Object

In general, nicotinic agonists improve certain forms of memory, and nicotinic antagonists and cholinergic lesions impair memory (5, 141–145). PubMed:17009926

Appears in Networks:

a(CHEBI:"nicotinic acetylcholine receptor agonist") increases bp(GO:memory) View Subject | View Object

In animal studies, acute and chronic nicotine administration improves working memory, and nicotinic agonists were found to improve learning and memory in humans and nonhuman primates (145). PubMed:17009926

Appears in Networks:

a(CHEBI:"nicotinic antagonist") decreases bp(GO:memory) View Subject | View Object

In general, nicotinic agonists improve certain forms of memory, and nicotinic antagonists and cholinergic lesions impair memory (5, 141–145). PubMed:17009926

Appears in Networks:

a(CHEBI:nicotine) increases bp(GO:memory) View Subject | View Object

In animal studies, acute and chronic nicotine administration improves working memory, and nicotinic agonists were found to improve learning and memory in humans and nonhuman primates (145). PubMed:17009926

Appears in Networks:

a(PUBCHEM:5311278) decreases bp(GO:memory) View Subject | View Object

For example, local infusion of the α7 antagonist, methyllycaconitine (MLA), or the β2∗ antagonist, dihydro-β-erythroidine (DHβE), into the basolateral amygdala, the ventral hippocampus, or the dorsal hippocampus impairs the working memory of rats seeking food reward within a 16-arm radial maze (146–148). PubMed:17009926

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
Hippocampus

p(FPLX:CHRN) association bp(GO:memory) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

Appears in Networks:

a(CHEBI:acetylcholine) positiveCorrelation bp(GO:memory) View Subject | View Object

Moreover, published data indicate that ACh is involved in memory PubMed:26813123

Appears in Networks:

a(CHEBI:acetylcholine) regulates bp(GO:memory) View Subject | View Object

Further studies have demonstrated that endogenous acetylcholine is important for modulation of acquisition [17], encoding [18], consolidation [19], reconsolidation [20], extinction [21] and retrieval of memory PubMed:26813123

Appears in Networks:

a(CHEBI:acetylcholine) association bp(GO:memory) View Subject | View Object

It has been demonstrated that the role of ACh in learning and memory seems to be related to the regulation of glutamatergic neurotransmission PubMed:26813123

Appears in Networks:

a(MESH:"Receptors, Cholinergic") increases bp(GO:memory) View Subject | View Object

Moreover, it has been shown that blocking CA3 cholinergic receptors impairs the encoding of information and memory PubMed:26813123

Appears in Networks:
Annotations
MeSH
CA3 Region, Hippocampal

a(CHEBI:xanomeline) increases bp(GO:memory) View Subject | View Object

In a large-scale placebo-controlled clinical trial, it was demonstrated that xanomeline, a muscarinic agonist with reasonable selectivity for M1/M4 receptors, exhibits a positive effect in minimizing, in a dose-dependent manner, cognitive and psychiatric symptoms in AD, including memory deficit, mood disturbance, agitation and hallucinations PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:"Cholinergic Neurons") positiveCorrelation bp(GO:memory) View Subject | View Object

The importance of the cholinergic neurons from the nucleus basalis of Meynert on memory is highlighted by the fact that the specific degeneration of these neurons takes place in Alzheimer’s disease (AD) and contributes to the memory loss exhibited by AD patients PubMed:26813123

Appears in Networks:
Annotations
MeSH
Basal Nucleus of Meynert

a(MESH:"Cholinergic Neurons") increases bp(GO:memory) View Subject | View Object

All these cholinergic alterations that take place in AD closely correlates with impaired attention and memory observed in patients PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:"Nerve Growth Factor") increases bp(GO:memory) View Subject | View Object

Moreover, previous studies have shown that treatment with NGF can counteract cholinergic atrophy and memory deficits in aged rats PubMed:26813123

Appears in Networks:

a(PUBCHEM:1476756) increases bp(GO:memory) View Subject | View Object

For example, it has been shown that the benzyl quinolone carboxylic acid (BQCA), which is an M1-selective allosteric agonist, is effective in increasing spontaneous excitatory postsynaptic currents in the medial prefrontal cortex (mPFC) pyramidal cells and improving memory in a transgenic mouse model of AD PubMed:26813123

Appears in Networks:
Annotations
MeSH
Pyramidal Cells
MeSH
Alzheimer Disease

bp(GO:"synaptic transmission, cholinergic") association bp(GO:memory) View Subject | View Object

The cholinergic system is involved in critical physiological processes, such as attention, learning, memory, stress response, wakefulness and sleep, and sensory information PubMed:26813123

Appears in Networks:

bp(HBP:Neurodegeneration) negativeCorrelation bp(GO:memory) View Subject | View Object

The importance of the cholinergic neurons from the nucleus basalis of Meynert on memory is highlighted by the fact that the specific degeneration of these neurons takes place in Alzheimer’s disease (AD) and contributes to the memory loss exhibited by AD patients PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(MESH:"Synaptic Transmission") association bp(GO:memory) View Subject | View Object

In fact, the memory deficit and neuropathology severity observed in patients exhibiting AD highly correlate with changes in hippocampal synaptic transmission, especially with changes in synaptophysin expression, a presynaptic vesicle protein PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(HGNC:SYP) association bp(GO:memory) View Subject | View Object

In fact, the memory deficit and neuropathology severity observed in patients exhibiting AD highly correlate with changes in hippocampal synaptic transmission, especially with changes in synaptophysin expression, a presynaptic vesicle protein PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:xanomeline) increases bp(GO:memory) View Subject | View Object

One example is xanomeline, an mAChR agonist with selectivity for the M1 and M4 subtypes. Xanomeline improves working memory in rodents and improves cognition and reduces psychotic episodes in AD patients, but it failed during phase-II clinical trial because of serious side-effects, probably due to simultaneous activation of M1 and M4 mAChRs (M4 > M1) PubMed:24590577

Appears in Networks:

a(CHEBI:"(-)-cotinine") increases bp(GO:memory) View Subject | View Object

Cotinine is a nicotine metabolite known for its positive effects on memory and attention and lower toxicity compared to nicotine (Hatsukami et al., 1997) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:"(S)-2-ethyl-8-methyl-1-thia-4,8-diazaspiro(4.5)decan-3-one") increases bp(GO:memory) View Subject | View Object

Chronic treatment with AF267B reduces Abeta plaques and tau hyperphosphorylation and rescues learning and memory impairments in 3×Tg AD mice PubMed:24590577

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:"1-((4-cyano-4-(pyridine-2-yl)piperidin-1-yl)methyl)-4-oxo-4H-quinolizine-3-carboxylic acid") increases bp(GO:memory) View Subject | View Object

In mice with scopolamine-induced deficits, PQCA, a selective M1 mAChR positive allosteric modulator[87], improves not only recognition memory, spatial working memory, and executive function, but also blood-flow in the frontal cortex, though the mechanism is not yet clear. PubMed:24590577

Appears in Networks:

p(HGNCGENEFAMILY:"Cholinergic receptors muscarinic") association bp(GO:memory) View Subject | View Object

Members of the mAChR family are widely expressed in various regions in the central nervous system (CNS) and in the peripheral system. They play crucial roles in diverse physiological processes such as memory, attention, nociception, motor control, sleep-wake cycles, and cardiovascular, renal, and gastrointestinal functions PubMed:24590577

Appears in Networks:

p(HGNC:CHRM1) association bp(GO:memory) View Subject | View Object

Among the mAChR family members, the M1 subtype makes up 50–60% of the total and is predominantly expressed in all major areas of the forebrain, including the hippocampus, cerebral cortex, corpus striatum, and thalamus[36-38]. M1 mAChR-knockout mice show a series of cognitive defi cits and impairments in long-term potentiation, indicating that the M1 subtype is physiologically linked to multiple functions such as synaptic plasticity, neuronal excitability, neuronal differentiation during early development, and learning and memory PubMed:24590577

Appears in Networks:

a(CHEBI:"amyloid-beta") increases bp(GO:memory) View Subject | View Object

An in vivo Abeta infusion in mice was able to enhance hippocampal dependent memory, highlighted with memory tasks such as the Morris water maze and contextual fear conditioning, which are both hippocampus dependent behavioural tasks (Puzzo et al.,2008) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Hippocampus

a(CHEBI:nicotine) increases bp(GO:memory) View Subject | View Object

Nicotine treatment improved the memory deficit, highlighted with the Morris water maze task. Surprisingly, this study showed a dose dependent increase of alpha7 nAChR, a result that is in contrast with the literature (Oddo et al., 2005) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") increases bp(GO:memory) View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

composite(a(CHEBI:simvastatin), p(MGI:App, frag("25_35"))) increases bp(GO:memory) View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"GW 3965") increases bp(GO:memory) View Subject | View Object

Significantly, a 4-month treatment of Tg2576 mice with GW3965 reduced plaque deposition by > 50% and improved contextual memory in these animals [13]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:"all-trans-retinoic acid") increases bp(GO:memory) View Subject | View Object

Treatment of 5-month-old APP/PS1 mice for 8 weeks with ATRA (20 mg/kg/day) resulted in significant decreases in Ab deposition and tau phosphorylation in these mice. Additionally, it attenuated memory deficits seen in the Morris water maze [77]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

a(CHEBI:pioglitazone) increases bp(GO:memory) View Subject | View Object

In this study, pioglitazone treatment was shown to improve memory and cognition in these patients [67,68]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:rosiglitazone) increases bp(GO:memory) View Subject | View Object

A Phase II clinical trial in which patients were treated with rosiglitazone for 6 months showed improvements in attention and memory retention, but only in patients who did not have an APOE4 allele. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

act(p(HGNC:NR1H3)) increases bp(GO:memory) View Subject | View Object

A different result was reported by Vanmierlo et al. who found that LXR agonist treatment resulted in restoration of memory, but did not find a change in plaque burden [48]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High

p(MGI:Tmem35a) increases bp(GO:memory) View Subject | View Object

A very recent study also reported memory defects in mice lacking NACHO/TMEM35 done by scientists unaware of NACHO’s role in controlling nAChRs (Kennedy et al., 2016) PubMed:28445721

Appears in Networks:

bp(GO:"synaptic transmission, cholinergic") association bp(GO:memory) View Subject | View Object

In 2011, we know that cholinergic actions in the brain govern various processes: cognition (attention and executive function) (Couey et al., 2007; Levin and Rezvani, 2007; Heath and Picciotto, 2009; Howe et al., 2010), learning and memory (Gould, 2006; Couey et al., 2007; Levin and Rezvani, 2007), mood (anxiety, depression) (Picciotto et al., 2008), reward (addiction, craving) (Tang and Dani, 2009), and sensory processing (Heath and Picciotto, 2009) PubMed:21482353

Appears in Networks:
Annotations
MeSH
Brain

p(MGI:Lynx1) decreases bp(GO:memory) View Subject | View Object

As a consequence of nAChR hypersensitivity, lynx1 knockout mice display increased levels of Ca2+ in neurons, enhancements in synaptic efficacy, and improved learning and memory functions (Miwa et al., 2006; Darvas et al., 2009; Tekinay et al., 2009) PubMed:21482353

Appears in Networks:

p(FPLX:CHRN) association bp(GO:memory) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

a(CHEBI:nicotine) increases bp(GO:memory) View Subject | View Object

The potential therapeutic benefit of nAChR stimulation in AD is based upon the fact that nicotine improves memory in animals, healthy subjects, and AD patients (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Rusted and Warburton 1992) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:nicotine) increases bp(GO:memory) View Subject | View Object

Acute administration of nicotine to AD patients has resulted in a measurable short-term improvement in learning, memory, and attentional performance (Jones et al 1992) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:119380) increases bp(GO:memory) View Subject | View Object

Recently, the nicotinic agonist ABT- 418 improved verbal learning and memory on a selective reminding task in AD patients (Potter et al 1999) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(DRUGBANK:Facinicline) increases bp(GO:memory) View Subject | View Object

Two partial agonists of alpha7 nAChRs, GTS-21 (also a strong alpha4beta2 antagonist) and MeM-3454 (also a strong 5-hydroxytryptamine type 3 receptor (5HT3) antagonist)149 (TABLe 1), further showed a procognitive action and, in preclinical studies, MeM-3454 enhanced episodic, spatial and working memory. PubMed:19721446

Appears in Networks:
Annotations
Text Location
Review

a(MESH:"3-(2,4-dimethoxybenzylidene)anabaseine") increases bp(GO:memory) View Subject | View Object

initially evaluated in normal subjects, GTS-21 was found to significantly improve attention and memory. in a second Phase i trial187, GTS-21 normalized P50 auditory gating in patients with schizophrenia. PubMed:19721446

Appears in Networks:
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Text Location
Review

a(MESH:"AR-R 17779") increases bp(GO:memory) View Subject | View Object

As expected, AR-R17779 — a selective partial alpha7 nAChR agonist — improved scopolamine-elicited deficits in social recognition, and the 24-hour memory retention interval in unimpaired animals. Repeated doses of AR-R17779 enhanced long-term learning and attenuated working-memory deficits in rats. PubMed:19721446

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Annotations
Text Location
Review

a(MESH:"Entorhinal Cortex") association bp(GO:memory) View Subject | View Object

Amyloid plaques form in the entorhinal cortex of patients with Alzheimer’s disease and this region, which connects the neocortex and the hippocampus, plays a crucial part in memory. it has been suggested that plaques in this region represent the lytic remnants of degenerated, Abeta1–42-burdened pyramidal neurons, and that amyloid internalization depends on alpha7 nAChR mediated Ca2+ entry162. Of interest, chronic nicotine treatment has been shown to reduce the plaque burden in animal models of Alzheimer’s disease123. PubMed:19721446

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Annotations
MeSH
Entorhinal Cortex
Text Location
Review

a(MESH:Hippocampus) association bp(GO:memory) View Subject | View Object

First, there is a high level of expression of alpha7 nAChRs in the hippocampus, a region that is known to be involved in memory formation. Second, gene knockout and antisense studies have shown a role for alpha7 nAChRs in learning and memory144–146, and specifically in attention and working–episodic memory147,148. Third, pharmacological studies have shown that a range of structurally diverse alpha7 nAChR-selective agonists or positive allosteric modulators improve the cognitive deficits that are associated with Alzheimer’s disease. PubMed:19721446

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Text Location
Review

p(HGNC:CHRNA7) association bp(GO:memory) View Subject | View Object

First, there is a high level of expression of alpha7 nAChRs in the hippocampus, a region that is known to be involved in memory formation. Second, gene knockout and antisense studies have shown a role for alpha7 nAChRs in learning and memory144–146, and specifically in attention and working–episodic memory147,148. Third, pharmacological studies have shown that a range of structurally diverse alpha7 nAChR-selective agonists or positive allosteric modulators improve the cognitive deficits that are associated with Alzheimer’s disease. PubMed:19721446

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Text Location
Review

act(p(HGNC:CHRNA7)) decreases bp(GO:memory) View Subject | View Object

By contrast, deleting the alpha7 nAChR subunit in a mouse model of Alzheimer’s disease that overexpresses a mutated form of the human amyloid precursor protein confers protection against memory loss and synaptic dysfunction, supporting a crucial role for alpha7 nAChR as a target288. PubMed:19721446

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MeSH
Alzheimer Disease
Text Location
Review

bp(GO:"synaptic transmission, cholinergic") increases bp(GO:memory) View Subject | View Object

One of the salient events at early stages of this disease (usually pre- clinical) is the impairment in hippocampus-based episodic memory which can be improved by enhancement of cholinergic transmission [191]. PubMed:22040696

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Annotations
MeSH
Hippocampus

path(MESH:"Alzheimer Disease") decreases bp(GO:memory) View Subject | View Object

One of the salient events at early stages of this disease (usually pre- clinical) is the impairment in hippocampus-based episodic memory which can be improved by enhancement of cholinergic transmission [191]. PubMed:22040696

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MeSH
Hippocampus

a(CHEBI:tanespimycin) increases bp(GO:memory) View Subject | View Object

The less cytotoxic analogue of geldanamycin, 17-AAG, has improved brain penetrance. It decreased Aβ levels 223 , improved memory 224 and lowered tau in transgenic AD mice 224 . 17-AAG also reduced α-synuclein oligomers in H4 cells 220 . PubMed:30116051

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MeSH
Alzheimer Disease

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") increases bp(GO:memory) View Subject | View Object

Interestingly, the UPS is important for elimination of tau and other neurotoxic proteins in post synaptic dendritic compartments (a key site of spreading), where it plays a more general role favouring synaptic plasticity, den- dritogenesis and memory formation 49,52 . PubMed:30116051

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MeSH
Dendrites

a(HBP:"Tau oligomers") decreases bp(GO:memory) View Subject | View Object

Further, mice injected with tau oligomers in the proximity of the hippocampus experienced immediate memory impairment (Lasagna-Reeves et al., 2011) PubMed:28420982

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Confidence
Medium
MeSH
Hippocampus

p(HGNC:PPID) increases bp(GO:memory) View Subject | View Object

CyP40 was recently shown to disaggregate tau fibrils in vitro and prevents toxic tau accumulation in vivo preserving memory, demonstrating a neuroprotective role for CyP40 in the brain (Baker et al., 2017). PubMed:29311797

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a(CHEBI:"(-)-epigallocatechin 3-gallate") positiveCorrelation bp(GO:memory) View Subject | View Object

Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333

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MeSH
Alzheimer Disease
MeSH
Down Syndrome

a(HBP:RGFP966) association bp(GO:memory) View Subject | View Object

RGFP966, a selective HDAC3 inhibitor, has been shown to affect sensory cortical plasticity and memory formation (Bieszczad et al., 2015). PubMed:28771976

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a(HBP:MPT0G211) increases bp(GO:memory) View Subject | View Object

These results clearly indicated that MPT0G211 can penetrate the BBB, where it potentially ameliorates learning and memory deficits. PubMed:29844403

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bp(MESH:"Long-Term Potentiation") positiveCorrelation bp(GO:memory) View Subject | View Object

Here we report abnormal acetylation of K274 and K281 on tau, identified in AD brains, promotes memory loss and disrupts synaptic plasticity by reducing postsynaptic KIdney/BRAin (KIBRA) protein, a memory-associated protein.Transgenic mice expressing human tau with lysine-to-glutamine mutations to mimic K274 and K281 acetylation (tauKQ) exhibit AD-related memory deficits and impaired hippocampal long-term potentiation (LTP). TauKQ reduces synaptic KIBRA levels and disrupts activity-induced postsynaptic actin remodeling and AMPA receptor insertion. The LTP deficit was rescued by promoting actin polymerization or by KIBRA expression. In AD patients with dementia, we found enhanced tau acetylation is linked to loss of KIBRA. PubMed:27041503

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p(MGI:Dyrk1a) negativeCorrelation bp(GO:memory) View Subject | View Object

Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333

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MeSH
Alzheimer Disease
MeSH
Down Syndrome

p(HGNC:GSK3B) negativeCorrelation bp(GO:memory) View Subject | View Object

Nuclear factor erythroid-2-related factor 2 (Nrf2) is a transcription factor known to increase the level of many antioxidants, including glutathione-S transferase (GST), and is negatively regulated by the activity of GSK-3β. Our results indicated the increased nuclear localization of Nrf2 and level of GST, suggesting the increased activity of the transcription factor as a result of GSK-3β suppression, consistent with the decreased oxidative stress observed. Consistent with the improved learning and memory, and consistent with GSK-3b being a tau kinase, we observed decreased tau phosphorylation in brain of GAO-treated SAMP8 mice compared to that of RAO-treated SAMP8 mice. PubMed:24355211

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p(HGNC:SIRT1) positiveCorrelation bp(GO:memory) View Subject | View Object

SIRT1 activation or elevation ameliorates pathology and neurodegeneration in AD (Qin et al., 2006; Kim et al., 2007). Loss of SIRT1 induces impairment of learning and memory (Gao et al., 2010; Michán et al., 2010). PubMed:29540553

Appears in Networks:

p(MGI:Sumo3) negativeCorrelation bp(GO:memory) View Subject | View Object

In 25-month-old mice, the number of errors and the latency in the learning phase negatively correlated with the Sumo3 level in the dorsal hippocampus. PubMed:21843595

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Uberon
hippocampal formation

g(HGNC:NLRP3) decreases bp(GO:memory) View Subject | View Object

Deficiency of the NLRP3 gene reduces Aβ deposition and plays a protective role on memory and behavior (Heneka et al.,2013) PubMed:24561250

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Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph

a(CHEBI:"okadaic acid") decreases bp(GO:memory) View Subject | View Object

Further experiments based on the injection of a PP2A inhibitor in the rat hippocampus demon- strated tau hyper-phosphorylation, and learning and memory deficits [49, 50]. PubMed:22299660

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MeSH
Hippocampus

sec(a(CHEBI:"amyloid-beta")) increases bp(GO:memory) View Subject | View Object

This inhibition of Aβ secretion during macroautophagy deficiency results in aberrant cytosolic accumulation of Aβ, which ultimately evokes neurodegeneration accompanied with memory loss. PubMed:29758300

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a(CHEBI:"amyloid-beta") decreases bp(GO:memory) View Subject | View Object

Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190

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a(HBP:AβOs) decreases bp(GO:memory) View Subject | View Object

Soluble Ab oligomers inhibit hippocampal long-term potentiation and alter memory and learning performance PubMed:22908190

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bp(GO:"lysosomal protein catabolic process") increases bp(GO:memory) View Subject | View Object

Stimulating lysosomal proteolytic efficiency in the TgCRND8 APP mouse model by deleting an endogenous inhibitor of lysosomal cysteine proteases (cystatin B) rescues lysosomal pathology, eliminates abnormal autolysosomal accumulation of autophagy substrates, including Ab, decreases Ab and amyloid deposition, and ameliorates learning and memory deficits (Yang et al. 2011) PubMed:22908190

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bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") association bp(GO:memory) View Subject | View Object

The UPS is also critically involved in learning and memory. PubMed:22908190

Appears in Networks:

bp(GO:endocytosis) increases bp(GO:memory) View Subject | View Object

Although key to the survival of all cells, endocytosis supports unique neuronal functions, including aspects of synaptic transmission and plasticity underlying memory and learning. PubMed:22908190

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p(HBP:"UBB+1") decreases bp(GO:memory) View Subject | View Object

Indeed, transgenic mice expressing UBB+1 have an impaired UPS and show contextual memory deficits in both water maze and fear conditioning paradigms, without specific neuropathological findings (Fischer et al. 2009). PubMed:22908190

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p(HGNC:RIN1) decreases bp(GO:memory) View Subject | View Object

Conversely, deletion of the neuronal rab5 GEF, rin1, reduces rab5 activation, increases LTP induction in the amygdala, and enhances fear learning and memory, most likely by increasing surface levels of AMPA receptors (Dhaka et al. 2003). PubMed:22908190

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MeSH
Amygdala

p(HGNC:UCHL1) increases bp(GO:memory) View Subject | View Object

Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190

Appears in Networks:

a(HBP:"Tau oligomers") decreases bp(GO:memory) View Subject | View Object

Recently, extracellular tau oligomers were shown to impair long term potentiation (LTP) and memory [40]. PubMed:28528849

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MeSH
Extracellular Space

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) decreases bp(GO:memory) View Subject | View Object

TauRDΔK comprises the structural elements required for the pathologic assembly of tau filaments, and it causes reversible memory deficits and synapse loss in regulatable transgenic mice [11,25]. PubMed:28528849

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p(HGNC:MAPT, var("p.Lys280del")) increases bp(GO:memory) View Subject | View Object

Remarkably, in two regulatable transgenic mouse models expressing human tau with the P301L mutation (rTg4510) or expressing the repeat domain of tau with the ΔK280 mutation, switching off tau expression improved memory impairment even though NFTs remained, clearly showing that tau aggregates are not sufficient for neurodegeneration and the cognitive effects that are typically observed in these models PubMed:26631930

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p(HGNC:MAPT, var("p.Pro301Leu")) increases bp(GO:memory) View Subject | View Object

Remarkably, in two regulatable transgenic mouse models expressing human tau with the P301L mutation (rTg4510) or expressing the repeat domain of tau with the ΔK280 mutation, switching off tau expression improved memory impairment even though NFTs remained, clearly showing that tau aggregates are not sufficient for neurodegeneration and the cognitive effects that are typically observed in these models PubMed:26631930

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complex(GO:"NF-kappaB complex") increases bp(GO:memory) View Subject | View Object

The molecular mechanisms underlying the aforementioned involvement of NF-κB proteins in learning and memory have not been completely comprehended, although recent evidence has implicated NF-κB – induced transcriptional activation of Protein Kinase A (PKA) catalytic subunit that culminates in activation of CREB (cyclic AMP-response element binding protein) signaling [77] which is regarded as the molecular switch that converts short-term memory to long-term memory PubMed:28745240

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MeSH
Alzheimer Disease

a(CHEBI:"N(5)-ethyl-L-glutamine") increases bp(GO:memory) View Subject | View Object

It considerably decreased A 1-42-stimulated memory disorders in mice [128]. PubMed:29179999

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MeSH
Alzheimer Disease

a(CHEBI:"alpha-tocopherol") increases bp(GO:memory) View Subject | View Object

Memory defi-ciencies were improved by -tocopherol in transgenic mice. PubMed:29179999

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a(CHEBI:lycopene) increases bp(GO:memory) View Subject | View Object

It improved ICV A 1-42-activated spatial learning, and memory deficiencies were ameliorated via the interference of NF-B signaling and the inhibition of inflammatory cytokines [155]. PubMed:29179999

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a(PUBCHEM:155160) increases bp(GO:memory) View Subject | View Object

Beneficial effects of 4-O-methylhonokinol on memory were observed by the reduction of Aaggregation in A 1-42-injected mice and memory-impaired mice with its anti-oxidative and anti-inflammatory qualities [141–143]. PubMed:29179999

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MeSH
Alzheimer Disease

a(PUBCHEM:24721561) increases bp(GO:memory) View Subject | View Object

Ginsenoside Rd showed neuro-protective effects with A 40 activated impairments in rat brains [225] and ameliorated learning and memory capability in APP transgenic mice, via reducing the activity of NF-B [226]. PubMed:29179999

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MeSH
Alzheimer Disease

a(PUBCHEM:442534) increases bp(GO:memory) View Subject | View Object

Paeoniflorin improved memory impairments and lowered A accumulation in APP/PS1 trans-genic mice [1]. PubMed:29179999

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MeSH
Alzheimer Disease

a(PUBCHEM:73078) increases bp(GO:memory) View Subject | View Object

It ameliorated spatial learning and memory disorder, which was caused by A 1-42 and was associated with the inter-ference of NF-B activity and the inhibition of IL-1 and TNF-expression [183]. PubMed:29179999

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a(CHEBI:"advanced glycation end-product") decreases bp(GO:memory) View Subject | View Object

AGEs induce tau hyperphosphorylation, memory deterioration, decline of synaptic proteins, and impairment of long-term potentiation in rats [10]. PubMed:27288790

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a(PUBCHEM:9832404) association bp(GO:memory) View Subject | View Object

We evaluated the 31 transcripts regulated at both tested ages (see above) and found that the most enriched modified functions were related to nervous system development and activity including synapse assembly, positive regulation of synaptic transmission, glutamatergic, regulation of synapse organization, regulation of cell communication, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) glutamate receptor clustering, learning or memory, social behavior, regulation of ion transport, vocalization behavior, and nervous system development (Figure 3, Supplemental Tables 11 and 12) PubMed:30106381

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p(HGNC:ADNP) association bp(GO:memory) View Subject | View Object

We evaluated the 31 transcripts regulated at both tested ages (see above) and found that the most enriched modified functions were related to nervous system development and activity including synapse assembly, positive regulation of synaptic transmission, glutamatergic, regulation of synapse organization, regulation of cell communication, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) glutamate receptor clustering, learning or memory, social behavior, regulation of ion transport, vocalization behavior, and nervous system development (Figure 3, Supplemental Tables 11 and 12) PubMed:30106381

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composite(a(CHEBI:chlorobutanol), a(PUBCHEM:9832404)) increases bp(GO:memory) View Subject | View Object

Adnp+/− mice compared with Adnp+/+ mice spent significantly shorter time periods in exploring the new objects, indicative of impaired memory, with intranasal NAP-CB treatment completely ameliorating this impairment (Fig. 2a, b). PubMed:30664622

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p(HGNC:ADNP, pmod(MESH:Haploinsufficiency)) decreases bp(GO:memory) View Subject | View Object

Adnp+/− mice compared with Adnp+/+ mice spent significantly shorter time periods in exploring the new objects, indicative of impaired memory, with intranasal NAP-CB treatment completely ameliorating this impairment (Fig. 2a, b). PubMed:30664622

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p(HGNC:ADNP) increases bp(GO:memory) View Subject | View Object

Adnp+/− mice compared with Adnp+/+ mice spent significantly shorter time periods in exploring the new objects, indicative of impaired memory, with intranasal NAP-CB treatment completely ameliorating this impairment (Fig. 2a, b). PubMed:30664622

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Out-Edges 33

bp(GO:memory) association composite(p(HGNC:MAPK1), p(HGNC:MAPK3)) View Subject | View Object

Which pathway is activated by Abeta depends upon the time of exposure to the amyloid peptide: chronic applications of oligomeric Abeta to hippocampal slice cultures activate the JNK/MAPK pathway but inhibit the ERK/MAPK pathway, whereas short-term applications of Abeta oligomers do not activate JNK (Bell et al., 2004). This may be one of the routes whereby Abeta impairs memory, because ERK-1 and ERK-2 play key roles in the signaling events central to memory (Satoh et al., 2007). PubMed:19293145

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MeSH
Hippocampus

bp(GO:memory) association a(MESH:"Cerebral Cortex") View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

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MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association path(MESH:"Alzheimer Disease") View Subject | View Object

Conversely, the most commonly associated symptoms of AD are cognitive in nature and include deficits in learning and memory. However, 50%–80% of AD patients display psychotic and behavioral disturbances that are correlated with poor social and functional outcomes PubMed:24511233

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bp(GO:memory) association a(MESH:Hippocampus) View Subject | View Object

The popular amyloid cascade hypothesis posits that the gradual build-up of Abeta plaques leads to neuronal inflammation, dysfunction, and, eventually, cell death. The two brain regions most critically affected by this degeneration are the cortex and hippocampus, both of which are involved in cognition, learning, and memory. PubMed:24511233

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Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association a(MESH:Hippocampus) View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association a(MESH:"Cerebral Cortex") View Subject | View Object

The popular amyloid cascade hypothesis posits that the gradual build-up of Abeta plaques leads to neuronal inflammation, dysfunction, and, eventually, cell death. The two brain regions most critically affected by this degeneration are the cortex and hippocampus, both of which are involved in cognition, learning, and memory. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association bp(GO:"long-term synaptic potentiation") View Subject | View Object

M1 mAChRs have been demonstrated to potentiate NMDA-receptor signaling in the hippocampus and cortex,48,49 brain areas intimately associated with learning and memory. In addition, M1 KO mice displayed reduced hippocampal long-term potentiation, a mechanism heavily implicated in learning and memory. Behaviorally, M1 KO animals display deficits in several medial prefrontal cortex-dependent cognitive tasks, including non-matching-to- sample, win-shift radial arm maze, and social discrimination tasks. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:memory) association a(MESH:"Prefrontal Cortex") View Subject | View Object

In brain slice electrophysiology studies, BQCA enhanced excitatory postsynaptic currents in medial prefrontal cortical neurons,69 an area critical for higher cognitive, learning, and memory functions.70 In pre-clinical animal studies, BQCA reversed scopolamine-impaired contextual fear conditioning and rescued medial prefrontal cortex-dependent discrimination reversal learning deficits in a transgenic mouse model of AD. PubMed:24511233

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MeSH
Prefrontal Cortex

bp(GO:memory) association p(FPLX:CHRN) View Subject | View Object

By modulating activity-dependent events, nAChRs participate in fundamental aspects of synaptic plasticity that are involved in attention, learning, memory, and development (3, 12–16). PubMed:17009926

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bp(GO:memory) association bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

The cholinergic system is involved in critical physiological processes, such as attention, learning, memory, stress response, wakefulness and sleep, and sensory information PubMed:26813123

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bp(GO:memory) positiveCorrelation a(CHEBI:acetylcholine) View Subject | View Object

Moreover, published data indicate that ACh is involved in memory PubMed:26813123

Appears in Networks:

bp(GO:memory) association a(CHEBI:acetylcholine) View Subject | View Object

It has been demonstrated that the role of ACh in learning and memory seems to be related to the regulation of glutamatergic neurotransmission PubMed:26813123

Appears in Networks:

bp(GO:memory) positiveCorrelation a(MESH:"Cholinergic Neurons") View Subject | View Object

The importance of the cholinergic neurons from the nucleus basalis of Meynert on memory is highlighted by the fact that the specific degeneration of these neurons takes place in Alzheimer’s disease (AD) and contributes to the memory loss exhibited by AD patients PubMed:26813123

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MeSH
Basal Nucleus of Meynert

bp(GO:memory) negativeCorrelation bp(HBP:Neurodegeneration) View Subject | View Object

The importance of the cholinergic neurons from the nucleus basalis of Meynert on memory is highlighted by the fact that the specific degeneration of these neurons takes place in Alzheimer’s disease (AD) and contributes to the memory loss exhibited by AD patients PubMed:26813123

Appears in Networks:
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MeSH
Alzheimer Disease

bp(GO:memory) association bp(MESH:"Synaptic Transmission") View Subject | View Object

In fact, the memory deficit and neuropathology severity observed in patients exhibiting AD highly correlate with changes in hippocampal synaptic transmission, especially with changes in synaptophysin expression, a presynaptic vesicle protein PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

bp(GO:memory) association p(HGNC:SYP) View Subject | View Object

In fact, the memory deficit and neuropathology severity observed in patients exhibiting AD highly correlate with changes in hippocampal synaptic transmission, especially with changes in synaptophysin expression, a presynaptic vesicle protein PubMed:26813123

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

bp(GO:memory) association p(HGNCGENEFAMILY:"Cholinergic receptors muscarinic") View Subject | View Object

Members of the mAChR family are widely expressed in various regions in the central nervous system (CNS) and in the peripheral system. They play crucial roles in diverse physiological processes such as memory, attention, nociception, motor control, sleep-wake cycles, and cardiovascular, renal, and gastrointestinal functions PubMed:24590577

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bp(GO:memory) association p(HGNC:CHRM1) View Subject | View Object

Among the mAChR family members, the M1 subtype makes up 50–60% of the total and is predominantly expressed in all major areas of the forebrain, including the hippocampus, cerebral cortex, corpus striatum, and thalamus[36-38]. M1 mAChR-knockout mice show a series of cognitive defi cits and impairments in long-term potentiation, indicating that the M1 subtype is physiologically linked to multiple functions such as synaptic plasticity, neuronal excitability, neuronal differentiation during early development, and learning and memory PubMed:24590577

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bp(GO:memory) association bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

In 2011, we know that cholinergic actions in the brain govern various processes: cognition (attention and executive function) (Couey et al., 2007; Levin and Rezvani, 2007; Heath and Picciotto, 2009; Howe et al., 2010), learning and memory (Gould, 2006; Couey et al., 2007; Levin and Rezvani, 2007), mood (anxiety, depression) (Picciotto et al., 2008), reward (addiction, craving) (Tang and Dani, 2009), and sensory processing (Heath and Picciotto, 2009) PubMed:21482353

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Annotations
MeSH
Brain

bp(GO:memory) association p(FPLX:CHRN) View Subject | View Object

Interestingly enough, a considerable body of evidence exists to suggest that the nAChRs are involved in cognitive and memory functions (Levin 2000; Newhouse and Kelton 2000; Newhouse et al 1997; Sahakian and Coull 1994) PubMed:11230871

Appears in Networks:

bp(GO:memory) association a(MESH:Hippocampus) View Subject | View Object

First, there is a high level of expression of alpha7 nAChRs in the hippocampus, a region that is known to be involved in memory formation. Second, gene knockout and antisense studies have shown a role for alpha7 nAChRs in learning and memory144–146, and specifically in attention and working–episodic memory147,148. Third, pharmacological studies have shown that a range of structurally diverse alpha7 nAChR-selective agonists or positive allosteric modulators improve the cognitive deficits that are associated with Alzheimer’s disease. PubMed:19721446

Appears in Networks:
Annotations
Text Location
Review

bp(GO:memory) association p(HGNC:CHRNA7) View Subject | View Object

First, there is a high level of expression of alpha7 nAChRs in the hippocampus, a region that is known to be involved in memory formation. Second, gene knockout and antisense studies have shown a role for alpha7 nAChRs in learning and memory144–146, and specifically in attention and working–episodic memory147,148. Third, pharmacological studies have shown that a range of structurally diverse alpha7 nAChR-selective agonists or positive allosteric modulators improve the cognitive deficits that are associated with Alzheimer’s disease. PubMed:19721446

Appears in Networks:
Annotations
Text Location
Review

bp(GO:memory) association a(MESH:"Entorhinal Cortex") View Subject | View Object

Amyloid plaques form in the entorhinal cortex of patients with Alzheimer’s disease and this region, which connects the neocortex and the hippocampus, plays a crucial part in memory. it has been suggested that plaques in this region represent the lytic remnants of degenerated, Abeta1–42-burdened pyramidal neurons, and that amyloid internalization depends on alpha7 nAChR mediated Ca2+ entry162. Of interest, chronic nicotine treatment has been shown to reduce the plaque burden in animal models of Alzheimer’s disease123. PubMed:19721446

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MeSH
Entorhinal Cortex
Text Location
Review

bp(GO:memory) positiveCorrelation a(CHEBI:"(-)-epigallocatechin 3-gallate") View Subject | View Object

Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333

Appears in Networks:
Annotations
MeSH
Alzheimer Disease
MeSH
Down Syndrome

bp(GO:memory) negativeCorrelation p(MGI:Dyrk1a) View Subject | View Object

Treatment with Dyrk1A inhibitor, green tea flavonol epigallocatechin-gallate (EGCG), from gestation to adulthood suppressed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains. PubMed:28775333

Appears in Networks:
Annotations
MeSH
Alzheimer Disease
MeSH
Down Syndrome

bp(GO:memory) negativeCorrelation p(HGNC:GSK3B) View Subject | View Object

Nuclear factor erythroid-2-related factor 2 (Nrf2) is a transcription factor known to increase the level of many antioxidants, including glutathione-S transferase (GST), and is negatively regulated by the activity of GSK-3β. Our results indicated the increased nuclear localization of Nrf2 and level of GST, suggesting the increased activity of the transcription factor as a result of GSK-3β suppression, consistent with the decreased oxidative stress observed. Consistent with the improved learning and memory, and consistent with GSK-3b being a tau kinase, we observed decreased tau phosphorylation in brain of GAO-treated SAMP8 mice compared to that of RAO-treated SAMP8 mice. PubMed:24355211

Appears in Networks:

bp(GO:memory) positiveCorrelation bp(MESH:"Long-Term Potentiation") View Subject | View Object

Here we report abnormal acetylation of K274 and K281 on tau, identified in AD brains, promotes memory loss and disrupts synaptic plasticity by reducing postsynaptic KIdney/BRAin (KIBRA) protein, a memory-associated protein.Transgenic mice expressing human tau with lysine-to-glutamine mutations to mimic K274 and K281 acetylation (tauKQ) exhibit AD-related memory deficits and impaired hippocampal long-term potentiation (LTP). TauKQ reduces synaptic KIBRA levels and disrupts activity-induced postsynaptic actin remodeling and AMPA receptor insertion. The LTP deficit was rescued by promoting actin polymerization or by KIBRA expression. In AD patients with dementia, we found enhanced tau acetylation is linked to loss of KIBRA. PubMed:27041503

Appears in Networks:

bp(GO:memory) positiveCorrelation p(HGNC:SIRT1) View Subject | View Object

SIRT1 activation or elevation ameliorates pathology and neurodegeneration in AD (Qin et al., 2006; Kim et al., 2007). Loss of SIRT1 induces impairment of learning and memory (Gao et al., 2010; Michán et al., 2010). PubMed:29540553

Appears in Networks:

bp(GO:memory) association a(HBP:RGFP966) View Subject | View Object

RGFP966, a selective HDAC3 inhibitor, has been shown to affect sensory cortical plasticity and memory formation (Bieszczad et al., 2015). PubMed:28771976

Appears in Networks:

bp(GO:memory) negativeCorrelation p(MGI:Sumo3) View Subject | View Object

In 25-month-old mice, the number of errors and the latency in the learning phase negatively correlated with the Sumo3 level in the dorsal hippocampus. PubMed:21843595

Appears in Networks:
Annotations
Uberon
hippocampal formation

bp(GO:memory) association bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") View Subject | View Object

The UPS is also critically involved in learning and memory. PubMed:22908190

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bp(GO:memory) association p(HGNC:ADNP) View Subject | View Object

We evaluated the 31 transcripts regulated at both tested ages (see above) and found that the most enriched modified functions were related to nervous system development and activity including synapse assembly, positive regulation of synaptic transmission, glutamatergic, regulation of synapse organization, regulation of cell communication, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) glutamate receptor clustering, learning or memory, social behavior, regulation of ion transport, vocalization behavior, and nervous system development (Figure 3, Supplemental Tables 11 and 12) PubMed:30106381

Appears in Networks:

bp(GO:memory) association a(PUBCHEM:9832404) View Subject | View Object

We evaluated the 31 transcripts regulated at both tested ages (see above) and found that the most enriched modified functions were related to nervous system development and activity including synapse assembly, positive regulation of synaptic transmission, glutamatergic, regulation of synapse organization, regulation of cell communication, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) glutamate receptor clustering, learning or memory, social behavior, regulation of ion transport, vocalization behavior, and nervous system development (Figure 3, Supplemental Tables 11 and 12) PubMed:30106381

Appears in Networks:

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.