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    Home > Active Ingredient News > Study of Nervous System > Scientists in China have found that inhibiting the occurrence of nerves in adults can improve cognitive function in mice with Alzheimer's disease

    Scientists in China have found that inhibiting the occurrence of nerves in adults can improve cognitive function in mice with Alzheimer's disease

    • Last Update: 2021-01-26
    • Source: Internet
    • Author: User
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    Alzheimer's disease (AD) is the most common neurodegenerative disease and a complex disease caused by multiple factors.
    main clinical manifestations of cognitive impairment, such as loss or even loss of learning and memory.
    the pathogenesis of AD is not yet clear, abnormal aggregation of amyloid protein (amyloid β, A-beta) in the brain is closely related to AD.
    , however, the mechanism of a beta aggregation leading to abnormal neuron activity and synhaptic dysfunction has yet to be further studied.
    recently, Sun Binggui's team from Zhejiang University's School of Brain Science and Brain Medicine found in their research that inhibiting adult neurogenesy improved learning and memory function in mice with Alzheimer's disease.
    the study, published in the journal Stem Cell Reports, was published by Ablating Adult Neural Stem Cells Improves Synaptic and Cognitive Functionsin Alzheimer's Models.
    In the study, researchers used special experimental methods to inhibit adult neural development in mouse models of Alzheimer's disease, and subsequent mouse behavioral tests showed that inhibition of adult neural development improved spatial learning and memory in Alzheimer's mice.
    and immuno-staining and biochemic tests showed that inhibiting adult nerve occurrence had no effect on shearing of A-beta plaques, soluble A-beta and happ.
    electrophysiological test suggests that inhibiting the occurrence of adult nerves can restore synactical transmission of tooth-like repartitional cells in mice with Alzheimer's disease.
    these results suggest that inhibiting adult neural development improves learning and memory function in AD mice, not due to a decrease in A-beta, but is associated with the recovery of synhaptic transmission in toothy back granulocyte cells.
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