The Role of Neurotrophin Signaling in Age-Related Cognitive Decline and Cognitive Diseases.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
13 Jul 2022
Historique:
received: 31 05 2022
revised: 08 07 2022
accepted: 11 07 2022
entrez: 27 7 2022
pubmed: 28 7 2022
medline: 29 7 2022
Statut: epublish

Résumé

Neurotrophins are a family of secreted proteins expressed in the peripheral nervous system and the central nervous system that support neuronal survival, synaptic plasticity, and neurogenesis. Brain-derived neurotrophic factor (BDNF) and its high affinity receptor TrkB are highly expressed in the cortical and hippocampal areas and play an essential role in learning and memory. The decline of cognitive function with aging is a major risk factor for cognitive diseases such as Alzheimer's disease. Therefore, an alteration of BDNF/TrkB signaling with aging and/or pathological conditions has been indicated as a potential mechanism of cognitive decline. In this review, we summarize the cellular function of neurotrophin signaling and review the current evidence indicating a pathological role of neurotrophin signaling, especially of BDNF/TrkB signaling, in the cognitive decline in aging and age-related cognitive diseases. We also review the therapeutic approach for cognitive decline by the upregulation of the endogenous BDNF/TrkB-system.

Identifiants

pubmed: 35887075
pii: ijms23147726
doi: 10.3390/ijms23147726
pmc: PMC9320180
pii:
doi:

Substances chimiques

Brain-Derived Neurotrophic Factor 0
Neurotrophin 3 0
Receptor, trkB EC 2.7.10.1

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science
ID : JSPS KAKENHI 20K06857
Organisme : Japan Society for the Promotion of Science
ID : JSPS KAKENHI 19K16263
Organisme : Japan Society for the Promotion of Science
ID : JSPS KAKENHI 22K15660

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Auteurs

Tadahiro Numakawa (T)

Department of Cell Modulation, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.

Haruki Odaka (H)

Cellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 6, Tsukuba 305-8566, Japan.

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Classifications MeSH