The Implication of Androgens in the Presence of Protein Kinase C to Repair Alzheimer’s Disease-Induced Cognitive Dysfunction
Adult
Aged
Aged, 80 and over
Aging
/ physiology
Alzheimer Disease
/ pathology
Amyloid Precursor Protein Secretases
/ metabolism
Amyloid beta-Peptides
/ metabolism
Androgens
/ metabolism
Aspartic Acid Endopeptidases
/ metabolism
Cognition
/ physiology
Cognitive Dysfunction
/ pathology
Cyclic AMP Response Element-Binding Protein
/ metabolism
Female
Hippocampus
/ metabolism
Humans
Learning
/ physiology
MAP Kinase Signaling System
/ physiology
Male
Middle Aged
Neoplasm Proteins
/ metabolism
Phosphorylation
Protein Kinase C
/ metabolism
Receptors for Activated C Kinase
/ metabolism
tau Proteins
/ metabolism
Androgens
Cognition
Hippocampus
Protein kinase C
Spatial memory
Journal
Iranian biomedical journal
ISSN: 2008-823X
Titre abrégé: Iran Biomed J
Pays: Iran
ID NLM: 9814853
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
entrez:
4
11
2019
pubmed:
5
11
2019
medline:
6
6
2020
Statut:
ppublish
Résumé
Aging, as a major risk factor of memory deficiency, affects neural signaling pathways in hippocampus. In particular, age-dependent androgens deficiency causes cognitive impairments. Several enzymes like protein kinase C (PKC) are involved in memory deficiency. Indeed, PKC regulatory process mediates α-secretase activation to cleave APP in β-amyloid cascade and tau proteins phosphorylation mechanism. Androgens and cortisol regulate PKC signaling pathways, affecting the modulation of receptor for activated C kinase 1. Mitogen-activated protein kinase/ERK signaling pathway depends on CREB activity in hippocampal neurons and is involved in regulatory processes via PKC and androgens. Therefore, testosterone and PKC contribute in the neuronal apoptosis. The present review summarizes the current status of androgens, PKC, and their influence on cognitive learning. Inconsistencies in experimental investigations related to this fundamental correlation are also discussed, with emphasis on the mentioned contributors as the probable potent candidates for learning and memory improvement.
Substances chimiques
Amyloid beta-Peptides
0
Androgens
0
CREB1 protein, human
0
Cyclic AMP Response Element-Binding Protein
0
Neoplasm Proteins
0
RACK1 protein, human
0
Receptors for Activated C Kinase
0
tau Proteins
0
Protein Kinase C
EC 2.7.11.13
Amyloid Precursor Protein Secretases
EC 3.4.-
Aspartic Acid Endopeptidases
EC 3.4.23.-
BACE1 protein, human
EC 3.4.23.46
Types de publication
Journal Article
Review
Langues
eng
Pagination
64-80Références
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