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P3‐144: RETINAL GANGLION CELL AND INNER PLEXIFORM LAYER THINNING IN ALZHEIMER'S DISEASE: MORPHOMETRIC ANALYSIS OF BIOMARKERS IN THE EYE FOR DEGENERATION IN THE BRAIN
Author(s) -
Asanad Samuel,
Ross-Cisneros Fred N.,
Barron Ernesto,
Sadun Alfredo A.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1501
Subject(s) - inner plexiform layer , ophthalmology , ganglion , outer plexiform layer , ganglion cell layer , retinal , medicine , retina , optical coherence tomography , anatomy , retinal ganglion cell , optic nerve , pathology , biology , neuroscience
proteins show distinct pathological changes which contribute to Nmethyl-D-aspartate (NMDA) and a-amino-3-hydroxy-5-methyl-4isoxazolepropionic acid (AMPA) receptor loss at the PSD in AD. Ab oligomers also can induce the loss of Na/K-ATPase activity at synapse, which lead to synaptic dysfunction.Methods:we used Ginsenosides to remove Ab oligomers and protect synaptic function to prevent AD development at early stage.WhenAPP/PS1ADmice at 3 months old were treated 10mg/Kg Ginsenosides each day for consecutive 3 months, multiple methods including water Maze and fear conditioning test, westernblot, immunocytochemistry were used to examine memory change of these mice and the relevant mechanism. Results:The results showed Ginsenosides can increase space memory function of APP/PS1 mice to obviously decrease the time for finding safe platform, the levels of Ab oligomers were significantly decrease and the levels of dentridic spines and Shank3 proteins were significantly increased in the brains of APP/PS1 mice to rescue the homeostasis of synapse, compared with these levels in brains of APP/PS1 mice without treatment, respectively, and Ginsenosides can increase immunological function and neuronal autophage to clean Ab oligomers, and protect Na/K-ATPases to restore synaptic homeostasis, preventing AD development. Conclusions: Ginsenosides could be used to protect synaptic dysfunction in the early of AD.