Genistein protects hippocampal neurons against injury by regulating calcium/calmodulin dependent protein kinase IV protein levels in Alzheimer's disease model rats

Genistein has a neuroprotective effect in Alzheimer's disease, but its mechanism of action needs further clarification. Accumulating evidence suggests that excessive phosphorylation of tau protein causes production of neurofibrillary tangles, which is one of the main pathological characteristic...

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Bibliographic Details
Published in:Neural regeneration research 2017-09, Vol.12 (9), p.1479-1484
Main Authors: Ye, Shu, Wang, Ting-Ting, Cai, Biao, Wang, Yan, Li, Jing, Zhan, Ji-Xian, Shen, Guo-Ming
Format: Article
Language:English
Subjects:
Alzheimer's disease
Apoptosis
Care and treatment
Development and progression
Disease prevention
Health aspects
Hippocampus (Brain)
Isoflavones
Kinases
Laboratory animals
Memory
Morphology
nerve regeneration
neurodegeneration
genistein
Alzheimer′s disease
neuroprotection
hippocampus
learning
memory
tau protein
CAMK4
CALM
CAMKK1
neural regeneration
Phosphorylation
Physiological aspects
Protein kinases
Proteins
Rodents
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Summary:Genistein has a neuroprotective effect in Alzheimer's disease, but its mechanism of action needs further clarification. Accumulating evidence suggests that excessive phosphorylation of tau protein causes production of neurofibrillary tangles, which is one of the main pathological characteristics of Alzheimer's disease, and tau protein can be phosphorylated by calcium/calmodulin dependent protein kinase IV (CAMK4). After 7 days of pre-administration of genistein (90 mg/kg), an Alzheimer's disease rat model was established using an intraperitoneal injection of D-galactose combined with an intracerebral injection of amyloid-β peptide (25-35). The rat was then continuously administered genistein (90 mg/kg) for 42 days. The Morris water maze test, western blotting and hematoxylin-eosin staining results showed that genistein significantly decreased the escape latency and increased the number of times crossing the platform, reduced p-tau, CALM, CAMKK1 and p-CAMK4 protein levels in the hippocampus, and alleviated hippocampal neuron damage. These findings indicate that genistein may play a neuroprotective role in Alzheimer's disease through regulating CAMK4 to modulate tau hyperphosphorylation.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.215260