Basal forebrain cholinergic system in the dementias: Vulnerability, resilience, and resistance.
Alzheimer Disease
/ metabolism
Animals
Basal Forebrain
/ metabolism
Choline O-Acetyltransferase
/ metabolism
Cholinergic Neurons
/ metabolism
Dementia
/ metabolism
Disease Susceptibility
/ metabolism
Frontotemporal Lobar Degeneration
/ metabolism
Humans
Lewy Body Disease
/ metabolism
Nerve Degeneration
/ metabolism
Receptors, Cholinergic
/ metabolism
Resilience, Psychological
Tauopathies
/ metabolism
Alzheimer's disease
TDP-43 proteinopathy
basal forebrain cholinergic neurons
diffuse lewy body disease
frontotemporal lobar degeneration
tauopathy
Journal
Journal of neurochemistry
ISSN: 1471-4159
Titre abrégé: J Neurochem
Pays: England
ID NLM: 2985190R
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
revised:
08
07
2021
received:
12
04
2021
accepted:
12
07
2021
pubmed:
18
7
2021
medline:
18
11
2021
entrez:
17
7
2021
Statut:
ppublish
Résumé
The basal forebrain cholinergic neurons (BFCN) provide the primary source of cholinergic innervation of the human cerebral cortex. They are involved in the cognitive processes of learning, memory, and attention. These neurons are differentially vulnerable in various neuropathologic entities that cause dementia. This review summarizes the relevance to BFCN of neuropathologic markers associated with dementias, including the plaques and tangles of Alzheimer's disease (AD), the Lewy bodies of diffuse Lewy body disease, the tauopathy of frontotemporal lobar degeneration (FTLD-TAU) and the TDP-43 proteinopathy of FTLD-TDP. Each of these proteinopathies has a different relationship to BFCN and their corticofugal axons. Available evidence points to early and substantial degeneration of the BFCN in AD and diffuse Lewy body disease. In AD, the major neurodegenerative correlate is accumulation of phosphotau in neurofibrillary tangles. However, these neurons are less vulnerable to the tauopathy of FTLD. An intriguing finding is that the intracellular tau of AD causes destruction of the BFCN, whereas that of FTLD does not. This observation has profound implications for exploring the impact of different species of tauopathy on neuronal survival. The proteinopathy of FTLD-TDP shows virtually no abnormal inclusions within the BFCN. Thus, the BFCN are highly vulnerable to the neurodegenerative effects of tauopathy in AD, resilient to the neurodegenerative effect of tauopathy in FTLD and apparently resistant to the emergence of proteinopathy in FTLD-TDP and perhaps also in Pick's disease. Investigations are beginning to shed light on the potential mechanisms of this differential vulnerability and their implications for therapeutic intervention.
Identifiants
pubmed: 34272732
doi: 10.1111/jnc.15471
pmc: PMC8458251
mid: NIHMS1725514
doi:
Substances chimiques
Receptors, Cholinergic
0
Choline O-Acetyltransferase
EC 2.3.1.6
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1394-1411Subventions
Organisme : NIA NIH HHS
ID : P30 AG013854
Pays : United States
Organisme : NIA NIH HHS
ID : K08 AG065463
Pays : United States
Organisme : NIDCD NIH HHS
ID : R01 DC008552
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001422
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG072977
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG062566
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS085770
Pays : United States
Informations de copyright
© 2021 International Society for Neurochemistry.
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