a(MESH:D059329)
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
Cholinergic basal forebrain (CBF) cortical projection neurons contain the pathological AD hallmark, neurofibrillary tangles (NFTs), and undergo chemical phenotypic alterations during the progression of AD, making them an excellent natural model for studying mechanisms of cell death, survival and treatment approaches both in vitro and in vivo, including relevant animal models of neurodegeneration as well as human postmortem clinical pathological tissue studies [14]. PubMed:18986241
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
For example, the neuropeptide GAL, which functions via the interaction with three G protein-coupled receptors termed GALR1, GALR2 and GALR3, has multiple biological actions, including effects on cognition and neuroplasticity [15,146,147]. In the late [148–150] but not early [151] stage of AD, fibers within the basal forebrain containing the neuropeptide GAL thicken and hyperinnervate surviving CBF neurons. Although animal and cell-culture studies have shown that GAL plays a crucial role in the regulation of CBF neuron activity [152] and rescues cholinergic cells from amyloid toxicity [153], the molecular consequences of this unique plasticity response upon CBF neurons in AD remain unclear. Gene expression studies of cholinergic transcripts have shown that GAL hyperinnervated, but not nonhyperinnervated, CBF neurons display an upregulation of ChAT expression in AD compared to controls [126] PubMed:18986241
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
Although there is a widespread decline in various neurotransmitter containing cell bodies in end-stage AD, the most consistent losses throughout the progression of AD are seen in long projection neurons, including cholinergic neurons of the basal forebrain [11–13] PubMed:18986241
Cholinergic basal forebrain (CBF) cortical projection neurons contain the pathological AD hallmark, neurofibrillary tangles (NFTs), and undergo chemical phenotypic alterations during the progression of AD, making them an excellent natural model for studying mechanisms of cell death, survival and treatment approaches both in vitro and in vivo, including relevant animal models of neurodegeneration as well as human postmortem clinical pathological tissue studies [14]. PubMed:18986241
Specifically, progressive phenotypic downregulation of markers within CBF neurons as well as frank CBF cell loss has been observed consistently, along with an associated reduction of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity within the cortex in AD [16]. Most researchers presumed that progressive disruption of cholinergic function underlies much of the short-term memory loss seen in AD PubMed:18986241
Cholinergic neurons within the nucleus basalis (NB) and the septal diagonal band complex provide the major source of cholinergic innervation to the cerebral cortex and hippocampus, respectively, and play a key role in memory and attentional function [11–13]. PubMed:18986241
Cholinergic neurons within the nucleus basalis (NB) and the septal diagonal band complex provide the major source of cholinergic innervation to the cerebral cortex and hippocampus, respectively, and play a key role in memory and attentional function [11–13]. PubMed:18986241
Notably, reports that physostigmine and oral anticholinesterases have beneficial effects for patients with AD suggest that the CBF system is somewhat preserved during the progression of dementia, despite well-documented loss of cholinergic biosynthetic machinery (including ChAT and AChE enzyme deficits) in patients with this disease. Interestingly, recent studies have shown that ChAT activity, which results in acetylcholine (ACh) synthesis, is preserved in the neocortex of people with MCI [18,19]. PubMed:18986241
Specifically, progressive phenotypic downregulation of markers within CBF neurons as well as frank CBF cell loss has been observed consistently, along with an associated reduction of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity within the cortex in AD [16]. Most researchers presumed that progressive disruption of cholinergic function underlies much of the short-term memory loss seen in AD PubMed:18986241
This increase in alpha7 nAChR expression levels within CBF neurons was inversely associated with cognitive performance. Increased alpha7 nAChR expression in CBF neurons may signal a compensatory response to maintain basocortical cholinergic activity during the onset of AD. Upregulation of the alpha7 nAChR within individual CBF neurons is also consistent with reports of increased alpha7 nAChR mRNA and protein expression levels in hippocampal neurons, astrocytes and peripheral blood leukocytes in AD [120–122]. The observed increase in alpha7 nAChR in early AD may regulate basocortical cholinergic tone through pre- and/or postsynaptic mechanisms within cholinergic NB neurons prior to their frank degeneration in the later stages of AD. PubMed:18986241
Cholinergic neurons within the nucleus basalis (NB) and the septal diagonal band complex provide the major source of cholinergic innervation to the cerebral cortex and hippocampus, respectively, and play a key role in memory and attentional function [11–13]. PubMed:18986241
Cholinergic neurons within the nucleus basalis (NB) and the septal diagonal band complex provide the major source of cholinergic innervation to the cerebral cortex and hippocampus, respectively, and play a key role in memory and attentional function [11–13]. PubMed:18986241
Cholinergic neurons within the nucleus basalis (NB) and the septal diagonal band complex provide the major source of cholinergic innervation to the cerebral cortex and hippocampus, respectively, and play a key role in memory and attentional function [11–13]. PubMed:18986241
Cholinergic basal forebrain (CBF) cortical projection neurons contain the pathological AD hallmark, neurofibrillary tangles (NFTs), and undergo chemical phenotypic alterations during the progression of AD, making them an excellent natural model for studying mechanisms of cell death, survival and treatment approaches both in vitro and in vivo, including relevant animal models of neurodegeneration as well as human postmortem clinical pathological tissue studies [14]. PubMed:18986241
Cholinergic basal forebrain (CBF) cortical projection neurons contain the pathological AD hallmark, neurofibrillary tangles (NFTs), and undergo chemical phenotypic alterations during the progression of AD, making them an excellent natural model for studying mechanisms of cell death, survival and treatment approaches both in vitro and in vivo, including relevant animal models of neurodegeneration as well as human postmortem clinical pathological tissue studies [14]. PubMed:18986241
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
The regions of the forebrain that contain cholinobasal and septohippocampal CBF neurons also display various non-cholinergic neurons, including GABAergic interneurons that innervate cholinergic perikarya [11]. In addition, neuropeptides often co-localize with CBF neurons. For example, the inhibitory neuropeptide galanin (GAL) is found in septohippocampal and NB neurons in rodents, but not in higher apes or humans where GAL fibers innvervate CBF neurons. [15]. PubMed:18986241
Specifically, progressive phenotypic downregulation of markers within CBF neurons as well as frank CBF cell loss has been observed consistently, along with an associated reduction of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activity within the cortex in AD [16]. Most researchers presumed that progressive disruption of cholinergic function underlies much of the short-term memory loss seen in AD PubMed:18986241
Notably, reports that physostigmine and oral anticholinesterases have beneficial effects for patients with AD suggest that the CBF system is somewhat preserved during the progression of dementia, despite well-documented loss of cholinergic biosynthetic machinery (including ChAT and AChE enzyme deficits) in patients with this disease. Interestingly, recent studies have shown that ChAT activity, which results in acetylcholine (ACh) synthesis, is preserved in the neocortex of people with MCI [18,19]. PubMed:18986241
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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.