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path(MESH:"Parkinson Disease")

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Entity

Name
Parkinson Disease
Namespace
mesh
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/mesh-names.belns

Appears in Networks 24

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

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

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

Nicotinic α4β2 acetylcholine receptors and cognitive function in Parkinson's disease 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

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

The Biology of Proteostasis in Aging and Disease v1.0.0

Alpha-synuclein oligomers: a new hope v1.0.0

Structural and functional properties of prefibrillar α-synuclein oligomers v1.0.0

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

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

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

Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation 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

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

Tau in physiology and pathology v1.0.0

New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

In-Edges 68

act(a(MESH:"Lymphatic Vessels")) association path(MESH:"Parkinson Disease") View Subject | View Object

Notably, although the fold change in significantly altered genes after lymphatic ablation and MWM was moderate (−1.79 < log2(fold change) < 1.69), functional enrichment analysis (Extended Data Fig. 5o, p) revealed changes in gene sets associated with neurodegenerative diseases, such as Huntington’s, Parkinson’s and Alzheimer’s disease (Extended Data Fig. 5o) PubMed:30046111

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Annotations
Confidence
High
MeSH
Meninges

a(CHEBI:dopamine) decreases path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

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Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

p(HBP:"alpha-6 alpha-4 beta-2 beta-3 nAChR", loc(MESH:"Basal Ganglia")) association path(MESH:"Parkinson Disease") View Subject | View Object

In the basal ganglia, including the ventral tegmental area (VTA) and substantia nigra, the alpha6 and possibly the beta3 nAChR subunits are included in alpha4beta2 nAChR complexes to generate highaffinity receptors. At present, this is the only brain area identified where alpha6 and beta3 are coexpressed with alpha4 and beta2 nAChR subunits. This finding is highly relevant for Parkinson’s disease (385, 386). PubMed:19126755

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Text Location
Review

path(MESH:"Muscle Rigidity") positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

path(MESH:"Tobacco Use Disorder") negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

However, epidemiological studies have reported that heavy smokers are less likely to experience PD (see reviews in Refs. 384, 385). PubMed:19126755

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Text Location
Review

path(MESH:Hypokinesia) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

path(MESH:Tremor) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons
Text Location
Review

act(p(FPLX:CHRN)) negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

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p(FPLX:CHRN) negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

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a(MESH:"Cholinergic Neurons") negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Further highlighting the importance of the cholinergic system in the CNS, cholinergic neuronal loss, especially in the basal forebrain, occurs not only in AD, but also in Parkinson’s disease [190, 191], Down syndrome [192], amyotrophic lateral sclerosis [193, 194], progressive supranuclear palsy [195, 196], and olivopontocerebellar atrophy [197] PubMed:26813123

Appears in Networks:
Annotations
MeSH
Basal Forebrain
MeSH
Central Nervous System

a(CHEBI:benzoxazine) decreases path(MESH:"Parkinson Disease") View Subject | View Object

M4 mAChR is also involved in the pathology of Parkinson’s disease, which is associated with the loss of dopaminergic neurons projecting to the striatum and an imbalance between cholinergic and dopaminergic systems. In the corpus striatum, M4 mAChR is closely co-localized with dopamine receptors on striatal-projecting neurons and the striatal M4 mAChR inhibits dopamine D1 receptor function. Mice lacking M4 mAChR show increased locomotor activity and enhanced dopamine D1 receptor-mediated effects[55]. Consequently, selective M4 mAChR antagonists, such as benzoxazines, have been developed for the treatment of Parkinson’s disease PubMed:24590577

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p(HGNC:CHRM4) association path(MESH:"Parkinson Disease") View Subject | View Object

M4 mAChR is also involved in the pathology of Parkinson’s disease, which is associated with the loss of dopaminergic neurons projecting to the striatum and an imbalance between cholinergic and dopaminergic systems. In the corpus striatum, M4 mAChR is closely co-localized with dopamine receptors on striatal-projecting neurons and the striatal M4 mAChR inhibits dopamine D1 receptor function. Mice lacking M4 mAChR show increased locomotor activity and enhanced dopamine D1 receptor-mediated effects[55]. Consequently, selective M4 mAChR antagonists, such as benzoxazines, have been developed for the treatment of Parkinson’s disease PubMed:24590577

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complex(HBP:"alpha-4 beta-2 nAChR") association path(MESH:"Parkinson Disease") View Subject | View Object

Furthermore, we studied in these 17 IPD patients (at Hoehn and Yahr stage 1 and 2) whether there were differences of the a4b2 nAchR densities in the brain hemisphere contralateral to the clinically more affected body side (=contralat- eral hemisphere) compared to the brain hemi- sphere ipsilateral to the clinically more affected body side (=ipsilateral hemisphere). PubMed:24762290

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path(MESH:Memory) association path(MESH:"Parkinson Disease") View Subject | View Object

We found high correlation coefficients for four brain regions (right superior parietal lobule, left thalamus, right pos- terior subcortical region, and left posterior subcor- tical region) and two CERAD subtests (Word List Intrusions and Boston Naming Test), some of them were statistically significant. PubMed:24762290

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path(MESH:"Tobacco Use") decreases path(MESH:"Parkinson Disease") View Subject | View Object

However, when all genetic factors are eliminated by studying monozygotic twins who are discordant for both tobacco use and Parkinson’s disease, tobacco smoking and chewing still decrease the risk of Parkinson’s disease (Tanner et al., 2002; Wirdefeldt et al., 2005) PubMed:21482353

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path(MESH:Smoking) decreases path(MESH:"Parkinson Disease") View Subject | View Object

However, when all genetic factors are eliminated by studying monozygotic twins who are discordant for both tobacco use and Parkinson’s disease, tobacco smoking and chewing still decrease the risk of Parkinson’s disease (Tanner et al., 2002; Wirdefeldt et al., 2005) PubMed:21482353

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p(FPLX:CHRN) association path(MESH:"Parkinson Disease") View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

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p(MESH:"Receptors, Nicotinic") association path(MESH:"Parkinson Disease") View Subject | View Object

nAChRs contribute to cognitive function, and changes in their number and/or func- tion are associated with various pathological conditions such as cognitive disorders, anxiety, depression, Alzheimer’s and Parkinson’s disease, pain and epilepsy PubMed:28901280

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a(MESH:"Lewy Bodies") association path(MESH:"Parkinson Disease") View Subject | View Object

The protofibrils can further aggregate and precipitate as amyloid fibrils that are present in Lewy bodies, the hallmark of sporadic, late-onset PD PubMed:14556719

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bp(GO:"neuron death") positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

In PD, the main neuropathological feature is the progressive death of neurons in the substantia nigra pars compacta with resulting loss of dopaminergic innervation of the striatum. PubMed:14556719

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Annotations
MeSH
Pars Compacta

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Several apparently independent aberrations linked to defects in the UPS have been described in various rare forms of hereditary PD PubMed:14556719

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bp(GO:"synaptic transmission, dopaminergic") negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

In PD, the main neuropathological feature is the progressive death of neurons in the substantia nigra pars compacta with resulting loss of dopaminergic innervation of the striatum. PubMed:14556719

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Annotations
MeSH
Pars Compacta

p(HGNC:PRKN) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

An important player in the pathogenesis of PD is Parkin (PARK2)) PubMed:14556719

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p(HGNC:SNCA, var("p.Ala30Pro")) association path(MESH:"Parkinson Disease") View Subject | View Object

In the late 1990s, it was reported that two mutations in the N-terminal domain of alphaSYN, A30P (Kruger et al., 1998) and A53T (Polymeropoulos et al., 1997), were associated with a rare form of autosomal-dominant familial PD PubMed:14556719

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p(HGNC:SNCA, var("p.Ala53Thr")) association path(MESH:"Parkinson Disease") View Subject | View Object

In the late 1990s, it was reported that two mutations in the N-terminal domain of alphaSYN, A30P (Kruger et al., 1998) and A53T (Polymeropoulos et al., 1997), were associated with a rare form of autosomal-dominant familial PD PubMed:14556719

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p(HGNC:UCHL1, var("?")) association path(MESH:"Parkinson Disease") View Subject | View Object

Recent findings in a German family with PD have revealed a mutation in the gene coding for the ubiquitin carboxy-terminal hydrolase UCH-L1 (Leroy et al., 1998). PubMed:14556719

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p(HGNC:UCHL1, var("p.Ile93Met")) association path(MESH:"Parkinson Disease") View Subject | View Object

Themutation inUCH-L1 that was found linked to PD was identified as I93M PubMed:14556719

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a(CHEBI:sirolimus) decreases path(MESH:"Parkinson Disease") View Subject | View Object

Treatment of cell, Drosophila, and mouse models of HD, SCA3/MJD, AD, PD, and ALS with the mTOR inhibitor rapamycin (or a derivative) reduces aggregation and suppresses disease (140– 143). PubMed:25784053

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Cell Ontology (CL)
motor neuron

a(HBP:HBP00016) increases path(MESH:"Parkinson Disease") View Subject | View Object

Not only did this discovery draw attention to aggregated forms of a-syn as mediators of Parkinson’s disease pathogenesis, but also opened the door to the use of a-syn detection techniques for diagnosis and staging. PubMed:28803412

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Confidence
Medium

a(HBP:HBP00093) increases path(MESH:"Parkinson Disease") View Subject | View Object

. Multiple lines of evidence now suggest that oligomeric species of a-syn, which are thought to precede the fibrillar aggregates found in Lewy bodies, are the culprits for neuronal degeneration in Parkinson’s disease PubMed:28803412

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Annotations
Confidence
Medium

a(HBP:HBP00093) biomarkerFor path(MESH:"Parkinson Disease") View Subject | View Object

Oligomeric detection may have uses as a diagnostic biomarker, as a biomarker of the progression of the disease, and in the future, perhaps as an index of response to novel therapies. PubMed:28803412

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Annotations
Confidence
High
MeSH
Microglia

a(HBP:HBP00093) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Elevated levels of a-syn oligomers were found in PD patients compared to controls or AD patients in brain homogenate, CSF and serum. PubMed:28803412

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Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum

p(HGNC:SNCA) association path(MESH:"Parkinson Disease") View Subject | View Object

Over the past two decades, the pre-synaptic protein alphasynuclein (a-syn) has been irrefutably tied to the neurodegenerative disorder Parkinson’s disease. PubMed:28803412

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Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.Ala30Pro")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

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Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.Ala53Glu")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

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Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.Ala53Thr")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

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Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.Glu46Lys")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.Gly51Asp")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:SNCA, var("p.His50Gln")) increases path(MESH:"Parkinson Disease") View Subject | View Object

the point mutation in SNCA (A53T) was demonstrated to cause autosomal dominant Parkinson’s disease [126] and several other point mutations (A30P, E46K, H50Q, G51D and A53E) have since been shown to cause familial forms of Parkinson’s disease and dementia with Lewy bodies (DLB) [4, 79, 84, 119, 129, 167]. PubMed:28803412

Appears in Networks:
Annotations
Confidence
Medium

a(HBP:HBP00016) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Parkinson’s disease (PD), Multiple System Atrophy (MSA) and Dementia with Lewy Bodies (DLB) are devastating synucleinopathies. The deposition of filamentous insoluble protein inclusions termed Lewy bodies and Lewy neurites whose main constituent is aggregated α -synuclein (α -syn) characterizes synucleinopathies. PubMed:27075649

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Annotations
Confidence
High
MeSH
Lewy Bodies

p(HGNC:GBA, var("?")) increases path(MESH:"Parkinson Disease") View Subject | View Object

Fourth, homozygous mutations of lyso- somal β-glucocerebrosidase (βGCase; also known as GBA) provoke the LSD Gaucher disease, which is linked to decreased ALN flux, α-synuclein accumulation and a fivefold increase in risk of PD 43 (Supplementary Box 1). PubMed:30116051

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MeSH
Parkinson Disease

p(HGNC:LRRK2, var("?")) association path(MESH:"Parkinson Disease") View Subject | View Object

Second, the GTPase leucine-rich repeat serine/threonine-protein kinase 2 (LRRK2) is the most commonly mutated protein in late-onset, familial PD. PubMed:30116051

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MeSH
Parkinson Disease

p(HGNC:PINK1, var("?")) association path(MESH:"Parkinson Disease") View Subject | View Object

First, autosomal recessive forms of early-onset PD are associated with mutations in PTEN-induced putative kinase protein 1 (PINK1) and the E3 ubiquitin-protein ligase parkin; these mutations lead to deficits in the mitophagic removal of damaged mitochondria 69,70 (BOX 2) . PubMed:30116051

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Annotations
MeSH
Parkinson Disease

p(HGNC:PRKN, var("?")) association path(MESH:"Parkinson Disease") View Subject | View Object

First, autosomal recessive forms of early-onset PD are associated with mutations in PTEN-induced putative kinase protein 1 (PINK1) and the E3 ubiquitin-protein ligase parkin; these mutations lead to deficits in the mitophagic removal of damaged mitochondria 69,70 (BOX 2) . PubMed:30116051

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Annotations
MeSH
Parkinson Disease

p(HGNC:STUB1) association path(MESH:"Parkinson Disease") View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

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MeSH
Cerebral Cortex

g(DBSNP:rs242557) association path(MESH:"Parkinson Disease") View Subject | View Object

A PSEN1 mutation causes a Pick’s disease phenotype including FTD tau pathology without deposition of Abeta [145]; some MAPT single nucleotide polymorphisms have also been linked to sporadic Parkinson’s disease (PD, [146]); PubMed:26751493

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g(DBSNP:rs2471738) association path(MESH:"Parkinson Disease") View Subject | View Object

A PSEN1 mutation causes a Pick’s disease phenotype including FTD tau pathology without deposition of Abeta [145]; some MAPT single nucleotide polymorphisms have also been linked to sporadic Parkinson’s disease (PD, [146]); PubMed:26751493

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p(HGNC:LRRK2) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Using mass spectrometry, we identified multiple sites on recombinant tau that are phosphorylated by LRRK2 in vitro, including pT149 and pT153, which are phospho-epitopes that to date have been largely unexplored. Importantly, we demonstrate that expression of transgenic LRRK2 in a mouse model of tauopathy increased the aggregation of insoluble tau and its phosphorylation at T149, T153, T205, and S199/S202/T205 epitopes. PubMed:24113872

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a(HBP:"protein aggregates") positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Overexpression of the HSPB8-BAG3 complex also stimulates autophagy and facilitates the clearance of mutated aggregation-prone proteins, the accumulation of which characterizes many neurodegenerative disorders such as Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis (Seidel et al., 2011). PubMed:22020111

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bp(GO:macroautophagy) negativeCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Finally, numerous studies using iPSC models have implicated changes in macroautophagy pathways in Parkinson’s disease [137–144], Gaucher disease [145], Niemann-Pick Type C1 disease [146–148] and diseases affecting motor neurons, including ALS [149,150], spinal and bulbar muscular atrophy (SBMA) [151], Brown- Vialetto disease [152], Charcot-Marie-Tooth 2A [153] and hereditary spastic paraplegia [154] PubMed:29758300

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p(HGNC:SNCA) increases path(MESH:"Parkinson Disease") View Subject | View Object

While misfolding of Aβ peptide and hyperphosphorylation of tau are recognized as pathogenic mechanisms of AD, accumulation of α-synuclein, which is recognized more as a risk factor for Parkinson’s disease (PD), also plays a pathological role in AD [29]. PubMed:29758300

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p(HGNC:VPS35, var("?")) association path(MESH:"Parkinson Disease") View Subject | View Object

VPS35 mutations have been shown to disrupt macroautophagy [113] and mitochondrial function [114] and are associated with AD and PD [102,115]. PubMed:29758300

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path(MESH:"Plaque, Amyloid") positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

Formation of amyloid β (Aβ) plaques is one of the most notable hallmarks in AD pathology [30] PubMed:29758300

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p(HGNC:SNCA, pmod(Ub)) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

In AD, tau is ubiquitinated, in Parkinson’s disease and dementia with Lewy bodies, it is a-synuclein, and in ALS and FTLD-U, it is TDP-43 PubMed:22908190

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p(HGNC:UCHL1) association path(MESH:"Parkinson Disease") View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

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a(GO:autophagosome) positiveCorrelation path(MESH:"Parkinson Disease") View Subject | View Object

This suggestion originates from the observed accumulation of autophagic vacuoles in neurons from affected brain regions in a number of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt- Jakob disease, and many of the polyglutamine diseases [21–24]. PubMed:18930136

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MeSH
Neurons

p(HGNC:SNCA, var("?")) increases path(MESH:"Parkinson Disease") View Subject | View Object

Mutations in α-synuclein that are causative of familial Parkinson’s disease are poorly transferred to the lysosomal lumen and accumulate on the lysosomal surface, resulting in blockade of receptor-mediated translocation. PubMed:18930136

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a(HBP:"alpha-synuclein aggregates") association path(MESH:"Parkinson Disease") View Subject | View Object

PD is a proteinopathy characterized by the misfolding and aggregation of α‐synuclein synucleinopathy, which leads to the destruction of dopaminergic neurons within substantia nigra pars compacta. PubMed:30663117

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MeSH
Parkinson Disease

a(HBP:"alpha-synuclein aggregates") increases path(MESH:"Parkinson Disease") View Subject | View Object

By linking to the 3′‐UTR sequence of Hsp70 mRNA, miR‐16‐1 configures Hsp70. Its increase reduces the Hsp70, which in turn boosts the aggregation of α‐synuclein protein, and this increases the incidence of PD. PubMed:30663117

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MeSH
Parkinson Disease

g(NCBIGENE:406950) association path(MESH:"Parkinson Disease") View Subject | View Object

miR‐16‐1 is a case in point that has been seen in some patients with PD.It has been shown to decrease the expression of Hsp70 by increasing the aggregation of the α‐synuclein protein PubMed:30663117

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Annotations
MeSH
Parkinson Disease

g(HGNC:"MIR153-1") decreases path(MESH:"Parkinson Disease") View Subject | View Object

That is, in the event that miRNAs regulating α‐synuclein that reduce its accumulation (including miR‐153, miR‐7, miR‐132, and miR‐133‐b) are decreased, the progression of PD will be accelerated. PubMed:30663117

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MeSH
Parkinson Disease

g(HGNC:"MIR7-1") decreases path(MESH:"Parkinson Disease") View Subject | View Object

That is, in the event that miRNAs regulating α‐synuclein that reduce its accumulation (including miR‐153, miR‐7, miR‐132, and miR‐133‐b) are decreased, the progression of PD will be accelerated. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:LRRK2) association path(MESH:"Parkinson Disease") View Subject | View Object

One of the most important proteins involved in PD is the LRRK2 protein PubMed:30663117

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MeSH
Parkinson Disease

g(HGNC:MIR132) association path(MESH:"Parkinson Disease") View Subject | View Object

However, this is part of the role that miR‐132 plays in the regulation of PD. PubMed:30663117

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MeSH
Parkinson Disease

g(HGNC:MIR132) decreases path(MESH:"Parkinson Disease") View Subject | View Object

That is, in the event that miRNAs regulating α‐synuclein that reduce its accumulation (including miR‐153, miR‐7, miR‐132, and miR‐133‐b) are decreased, the progression of PD will be accelerated. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Parkinson Disease

g(HGNC:MIR133B) decreases path(MESH:"Parkinson Disease") View Subject | View Object

That is, in the event that miRNAs regulating α‐synuclein that reduce its accumulation (including miR‐153, miR‐7, miR‐132, and miR‐133‐b) are decreased, the progression of PD will be accelerated. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Parkinson Disease

p(HGNC:LRRK2, var("p.Gly2019Ser")) increases path(MESH:"Parkinson Disease") View Subject | View Object

One of the most important mutations in LRRK2 is the Gly2019- Ser mutant, the most common cause of familial PD. PubMed:30663117

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MeSH
Parkinson Disease

p(HGNC:SNCA, var("?")) increases path(MESH:"Parkinson Disease") View Subject | View Object

The mutation in the SNCA gene causes PD. PubMed:30663117

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MeSH
Parkinson Disease

Out-Edges 53

path(MESH:"Parkinson Disease") association act(a(MESH:"Lymphatic Vessels")) View Subject | View Object

Notably, although the fold change in significantly altered genes after lymphatic ablation and MWM was moderate (−1.79 < log2(fold change) < 1.69), functional enrichment analysis (Extended Data Fig. 5o, p) revealed changes in gene sets associated with neurodegenerative diseases, such as Huntington’s, Parkinson’s and Alzheimer’s disease (Extended Data Fig. 5o) PubMed:30046111

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Confidence
High
MeSH
Meninges

path(MESH:"Parkinson Disease") association p(HGNC:UCHL1, var("p.Ile93Met")) View Subject | View Object

Themutation inUCH-L1 that was found linked to PD was identified as I93M PubMed:14556719

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path(MESH:"Parkinson Disease") negativeCorrelation path(MESH:"Tobacco Use Disorder") View Subject | View Object

However, epidemiological studies have reported that heavy smokers are less likely to experience PD (see reviews in Refs. 384, 385). PubMed:19126755

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Text Location
Review

path(MESH:"Parkinson Disease") association p(HBP:"alpha-6 alpha-4 beta-2 beta-3 nAChR", loc(MESH:"Basal Ganglia")) View Subject | View Object

In the basal ganglia, including the ventral tegmental area (VTA) and substantia nigra, the alpha6 and possibly the beta3 nAChR subunits are included in alpha4beta2 nAChR complexes to generate highaffinity receptors. At present, this is the only brain area identified where alpha6 and beta3 are coexpressed with alpha4 and beta2 nAChR subunits. This finding is highly relevant for Parkinson’s disease (385, 386). PubMed:19126755

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Review

path(MESH:"Parkinson Disease") positiveCorrelation path(MESH:Tremor) View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

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MeSH
Dopaminergic Neurons
Text Location
Review

path(MESH:"Parkinson Disease") positiveCorrelation path(MESH:Hypokinesia) View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

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MeSH
Dopaminergic Neurons
Text Location
Review

path(MESH:"Parkinson Disease") positiveCorrelation path(MESH:"Muscle Rigidity") View Subject | View Object

Parkinson’s disease (PD) is characterized by selective damage to dopaminergic nigrostriatal neurons and is clinically revealed by motor deficits, including rigidity, tremor, and bradykinesia. Dopamine replacement therapy (usually with L-dopa) is the most common treatment, although this drug loses efficacy over time. PubMed:19126755

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MeSH
Dopaminergic Neurons
Text Location
Review

path(MESH:"Parkinson Disease") negativeCorrelation act(p(FPLX:CHRN)) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

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path(MESH:"Parkinson Disease") negativeCorrelation p(FPLX:CHRN) View Subject | View Object

Nicotinic mechanisms contribute to cognitive function, and the decline of nicotinic mechanisms or loss of nAChRs has been observed in AD, dementia with Lewy bodies, Down syndrome, autism, and Parkinson’s disease (20, 140). PubMed:17009926

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path(MESH:"Parkinson Disease") negativeCorrelation a(MESH:"Cholinergic Neurons") View Subject | View Object

Further highlighting the importance of the cholinergic system in the CNS, cholinergic neuronal loss, especially in the basal forebrain, occurs not only in AD, but also in Parkinson’s disease [190, 191], Down syndrome [192], amyotrophic lateral sclerosis [193, 194], progressive supranuclear palsy [195, 196], and olivopontocerebellar atrophy [197] PubMed:26813123

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MeSH
Basal Forebrain
MeSH
Central Nervous System

path(MESH:"Parkinson Disease") association p(HGNC:CHRM4) View Subject | View Object

M4 mAChR is also involved in the pathology of Parkinson’s disease, which is associated with the loss of dopaminergic neurons projecting to the striatum and an imbalance between cholinergic and dopaminergic systems. In the corpus striatum, M4 mAChR is closely co-localized with dopamine receptors on striatal-projecting neurons and the striatal M4 mAChR inhibits dopamine D1 receptor function. Mice lacking M4 mAChR show increased locomotor activity and enhanced dopamine D1 receptor-mediated effects[55]. Consequently, selective M4 mAChR antagonists, such as benzoxazines, have been developed for the treatment of Parkinson’s disease PubMed:24590577

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path(MESH:"Parkinson Disease") decreases act(a(MESH:"Dopaminergic Neurons")) View Subject | View Object

M4 mAChR is also involved in the pathology of Parkinson’s disease, which is associated with the loss of dopaminergic neurons projecting to the striatum and an imbalance between cholinergic and dopaminergic systems. In the corpus striatum, M4 mAChR is closely co-localized with dopamine receptors on striatal-projecting neurons and the striatal M4 mAChR inhibits dopamine D1 receptor function. Mice lacking M4 mAChR show increased locomotor activity and enhanced dopamine D1 receptor-mediated effects[55]. Consequently, selective M4 mAChR antagonists, such as benzoxazines, have been developed for the treatment of Parkinson’s disease PubMed:24590577

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path(MESH:"Parkinson Disease") decreases path(MESH:Memory) View Subject | View Object

Performance was impaired, compared with a normal population, in the subtests Figure Recall and Figure Saving. These both subtests examined non-verbal functions, namely non-verbal memory and visuoconstructive ability. PubMed:24762290

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path(MESH:"Parkinson Disease") association path(MESH:Memory) View Subject | View Object

We found high correlation coefficients for four brain regions (right superior parietal lobule, left thalamus, right pos- terior subcortical region, and left posterior subcor- tical region) and two CERAD subtests (Word List Intrusions and Boston Naming Test), some of them were statistically significant. PubMed:24762290

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path(MESH:"Parkinson Disease") association complex(HBP:"alpha-4 beta-2 nAChR") View Subject | View Object

Furthermore, we studied in these 17 IPD patients (at Hoehn and Yahr stage 1 and 2) whether there were differences of the a4b2 nAchR densities in the brain hemisphere contralateral to the clinically more affected body side (=contralat- eral hemisphere) compared to the brain hemi- sphere ipsilateral to the clinically more affected body side (=ipsilateral hemisphere). PubMed:24762290

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path(MESH:"Parkinson Disease") association a(MESH:"Lewy Bodies") View Subject | View Object

The protofibrils can further aggregate and precipitate as amyloid fibrils that are present in Lewy bodies, the hallmark of sporadic, late-onset PD PubMed:14556719

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path(MESH:"Parkinson Disease") association p(FPLX:CHRN) View Subject | View Object

The nAChRs are found to be involved in a complex range of central nervous system disorders including Alzheimer’s disease (AD), Parkinson’s disease, schizophrenia, Tourette’s syndrome, anxiety, depression, and epilepsy (Newhouse and Kelton 2000; Newhouse et al 1997; Paterson and Nordberg 2000) PubMed:11230871

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path(MESH:"Parkinson Disease") association p(MESH:"Receptors, Nicotinic") View Subject | View Object

nAChRs contribute to cognitive function, and changes in their number and/or func- tion are associated with various pathological conditions such as cognitive disorders, anxiety, depression, Alzheimer’s and Parkinson’s disease, pain and epilepsy PubMed:28901280

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path(MESH:"Parkinson Disease") association p(HGNC:UCHL1, var("?")) View Subject | View Object

Recent findings in a German family with PD have revealed a mutation in the gene coding for the ubiquitin carboxy-terminal hydrolase UCH-L1 (Leroy et al., 1998). PubMed:14556719

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path(MESH:"Parkinson Disease") positiveCorrelation bp(GO:"neuron death") View Subject | View Object

In PD, the main neuropathological feature is the progressive death of neurons in the substantia nigra pars compacta with resulting loss of dopaminergic innervation of the striatum. PubMed:14556719

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MeSH
Pars Compacta

path(MESH:"Parkinson Disease") negativeCorrelation bp(GO:"synaptic transmission, dopaminergic") View Subject | View Object

In PD, the main neuropathological feature is the progressive death of neurons in the substantia nigra pars compacta with resulting loss of dopaminergic innervation of the striatum. PubMed:14556719

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MeSH
Pars Compacta

path(MESH:"Parkinson Disease") negativeCorrelation bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") View Subject | View Object

Several apparently independent aberrations linked to defects in the UPS have been described in various rare forms of hereditary PD PubMed:14556719

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path(MESH:"Parkinson Disease") positiveCorrelation p(HGNC:PRKN) View Subject | View Object

An important player in the pathogenesis of PD is Parkin (PARK2)) PubMed:14556719

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path(MESH:"Parkinson Disease") association p(HGNC:SNCA, var("p.Ala30Pro")) View Subject | View Object

In the late 1990s, it was reported that two mutations in the N-terminal domain of alphaSYN, A30P (Kruger et al., 1998) and A53T (Polymeropoulos et al., 1997), were associated with a rare form of autosomal-dominant familial PD PubMed:14556719

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path(MESH:"Parkinson Disease") association p(HGNC:SNCA, var("p.Ala53Thr")) View Subject | View Object

In the late 1990s, it was reported that two mutations in the N-terminal domain of alphaSYN, A30P (Kruger et al., 1998) and A53T (Polymeropoulos et al., 1997), were associated with a rare form of autosomal-dominant familial PD PubMed:14556719

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path(MESH:"Parkinson Disease") positiveCorrelation a(HBP:HBP00093) View Subject | View Object

Elevated levels of a-syn oligomers were found in PD patients compared to controls or AD patients in brain homogenate, CSF and serum. PubMed:28803412

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Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum

path(MESH:"Parkinson Disease") association p(HGNC:SNCA) View Subject | View Object

Over the past two decades, the pre-synaptic protein alphasynuclein (a-syn) has been irrefutably tied to the neurodegenerative disorder Parkinson’s disease. PubMed:28803412

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Confidence
Medium

path(MESH:"Parkinson Disease") positiveCorrelation a(HBP:HBP00016) View Subject | View Object

Parkinson’s disease (PD), Multiple System Atrophy (MSA) and Dementia with Lewy Bodies (DLB) are devastating synucleinopathies. The deposition of filamentous insoluble protein inclusions termed Lewy bodies and Lewy neurites whose main constituent is aggregated α -synuclein (α -syn) characterizes synucleinopathies. PubMed:27075649

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Confidence
High
MeSH
Lewy Bodies

path(MESH:"Parkinson Disease") association p(HGNC:PINK1, var("?")) View Subject | View Object

First, autosomal recessive forms of early-onset PD are associated with mutations in PTEN-induced putative kinase protein 1 (PINK1) and the E3 ubiquitin-protein ligase parkin; these mutations lead to deficits in the mitophagic removal of damaged mitochondria 69,70 (BOX 2) . PubMed:30116051

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") association p(HGNC:PRKN, var("?")) View Subject | View Object

First, autosomal recessive forms of early-onset PD are associated with mutations in PTEN-induced putative kinase protein 1 (PINK1) and the E3 ubiquitin-protein ligase parkin; these mutations lead to deficits in the mitophagic removal of damaged mitochondria 69,70 (BOX 2) . PubMed:30116051

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") association p(HGNC:LRRK2, var("?")) View Subject | View Object

Second, the GTPase leucine-rich repeat serine/threonine-protein kinase 2 (LRRK2) is the most commonly mutated protein in late-onset, familial PD. PubMed:30116051

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") increases path(MESH:"Proteostasis Deficiencies") View Subject | View Object

It is well accepted that loss of proteostasis occurs gradually with age and underlies the basis of severe neurodegenerative disorders such as Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and other types of frontotemporal dementia (Prahlad & Morimoto, 2009; Voisine et al., 2010; Morimoto & Cuervo, 2014) PubMed:29024336

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Confidence
High
MeSH
Brain
MeSH
Neurons

path(MESH:"Parkinson Disease") association p(HGNC:STUB1) View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

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MeSH
Cerebral Cortex

path(MESH:"Parkinson Disease") association g(DBSNP:rs2471738) View Subject | View Object

A PSEN1 mutation causes a Pick’s disease phenotype including FTD tau pathology without deposition of Abeta [145]; some MAPT single nucleotide polymorphisms have also been linked to sporadic Parkinson’s disease (PD, [146]); PubMed:26751493

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path(MESH:"Parkinson Disease") association g(DBSNP:rs242557) View Subject | View Object

A PSEN1 mutation causes a Pick’s disease phenotype including FTD tau pathology without deposition of Abeta [145]; some MAPT single nucleotide polymorphisms have also been linked to sporadic Parkinson’s disease (PD, [146]); PubMed:26751493

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path(MESH:"Parkinson Disease") positiveCorrelation p(HGNC:LRRK2) View Subject | View Object

Using mass spectrometry, we identified multiple sites on recombinant tau that are phosphorylated by LRRK2 in vitro, including pT149 and pT153, which are phospho-epitopes that to date have been largely unexplored. Importantly, we demonstrate that expression of transgenic LRRK2 in a mouse model of tauopathy increased the aggregation of insoluble tau and its phosphorylation at T149, T153, T205, and S199/S202/T205 epitopes. PubMed:24113872

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path(MESH:"Parkinson Disease") positiveCorrelation a(HBP:"protein aggregates") View Subject | View Object

Overexpression of the HSPB8-BAG3 complex also stimulates autophagy and facilitates the clearance of mutated aggregation-prone proteins, the accumulation of which characterizes many neurodegenerative disorders such as Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis (Seidel et al., 2011). PubMed:22020111

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path(MESH:"Parkinson Disease") positiveCorrelation path(MESH:"Plaque, Amyloid") View Subject | View Object

Formation of amyloid β (Aβ) plaques is one of the most notable hallmarks in AD pathology [30] PubMed:29758300

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path(MESH:"Parkinson Disease") association p(HGNC:VPS35, var("?")) View Subject | View Object

VPS35 mutations have been shown to disrupt macroautophagy [113] and mitochondrial function [114] and are associated with AD and PD [102,115]. PubMed:29758300

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path(MESH:"Parkinson Disease") negativeCorrelation bp(GO:macroautophagy) View Subject | View Object

Finally, numerous studies using iPSC models have implicated changes in macroautophagy pathways in Parkinson’s disease [137–144], Gaucher disease [145], Niemann-Pick Type C1 disease [146–148] and diseases affecting motor neurons, including ALS [149,150], spinal and bulbar muscular atrophy (SBMA) [151], Brown- Vialetto disease [152], Charcot-Marie-Tooth 2A [153] and hereditary spastic paraplegia [154] PubMed:29758300

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path(MESH:"Parkinson Disease") positiveCorrelation p(HGNC:SNCA, pmod(Ub)) View Subject | View Object

In AD, tau is ubiquitinated, in Parkinson’s disease and dementia with Lewy bodies, it is a-synuclein, and in ALS and FTLD-U, it is TDP-43 PubMed:22908190

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path(MESH:"Parkinson Disease") association p(HGNC:UCHL1) View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

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path(MESH:"Parkinson Disease") positiveCorrelation a(GO:autophagosome) View Subject | View Object

This suggestion originates from the observed accumulation of autophagic vacuoles in neurons from affected brain regions in a number of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt- Jakob disease, and many of the polyglutamine diseases [21–24]. PubMed:18930136

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MeSH
Neurons

path(MESH:"Parkinson Disease") increases a(CHEBI:"iron(0)") View Subject | View Object

Notably, this accumulation of iron was observed in the brain regions with reduced soluble tau levels, such as the cortex in AD, the substantia nigra in PD and various brain regions in several other tauopathies PubMed:26631930

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MeSH
Substantia Nigra

path(MESH:"Parkinson Disease") association a(HBP:"alpha-synuclein aggregates") View Subject | View Object

PD is a proteinopathy characterized by the misfolding and aggregation of α‐synuclein synucleinopathy, which leads to the destruction of dopaminergic neurons within substantia nigra pars compacta. PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") association g(HGNC:MIR132) View Subject | View Object

However, this is part of the role that miR‐132 plays in the regulation of PD. PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") association g(NCBIGENE:406950) View Subject | View Object

miR‐16‐1 is a case in point that has been seen in some patients with PD.It has been shown to decrease the expression of Hsp70 by increasing the aggregation of the α‐synuclein protein PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") association p(HGNC:LRRK2) View Subject | View Object

One of the most important proteins involved in PD is the LRRK2 protein PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") decreases g(HGNC:MIR205) View Subject | View Object

It has also been shown that miR‐205 can regulate LRRK2 and that PD is associated with a significant reduction in the level of miR‐205 in the frontal cortex and striatum PubMed:30663117

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MeSH
Corpus Striatum
MeSH
Frontal Lobe
MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") decreases p(HGNC:PARK7) View Subject | View Object

It has been shown that DJ‐1 protein levels in patients with PD are significantly lower compared with the healthy subjects PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") increases g(HGNC:MIR494) View Subject | View Object

It has also been shown that miR‐494 in patients with PD increases significantly in comparison with healthy subjects. PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") decreases g(HGNC:MIR34B) View Subject | View Object

In addition, miR‐34‐b and miR‐34‐c have been shown to experience a significant reduction in patients with Parkinson’s compared with controls, and this reduction is accompanied by a decrease in the expression of DJ‐1 protein PubMed:30663117

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MeSH
Parkinson Disease

path(MESH:"Parkinson Disease") decreases g(HGNC:MIR34C) View Subject | View Object

In addition, miR‐34‐b and miR‐34‐c have been shown to experience a significant reduction in patients with Parkinson’s compared with controls, and this reduction is accompanied by a decrease in the expression of DJ‐1 protein PubMed:30663117

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MeSH
Parkinson Disease

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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.