Treatment for Alzheimer's disease
Alzheimer's Disease
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Alzheimer's disease is the commonest form of dementia in aged population. One of characteristic hall mark pathology is the accumulation of beta amyloid plaques.
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The accumulation of beta amyloid aggregates may result from the hypofunction of brain lysosomes that commonly occurs in aging
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Various drugs aimed at reducing beta-amyloid accumulation are currently undergoing clinical trials.
Zincure's Strategy for Treating Neurodegenerative Disease
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ZCS1 facilitates the migration of Zn²+ ions into intracellular lysosomes through endocytosis.
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Endocytoisis with Zn²+ induces TFEB activation, leading to increased expression of Cathepsin B/D and v-ATPase.
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Elevated Zn²+ levels within lysosomes trigger v-ATPase activation, resulting in a decrease in pH.
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These cellular responses promote the degradation of toxic protein aggregates, such as pTau or TDP-43, by autolysosomes and lysosomes.
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This process normalizes autophagic flux by enhancing both the quality and quantity of lysosomes.
5XFAD mouse model (Morris Water Maze test)
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Using Genetically Engineered Alzheimer's Mice
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Testing Spatial Memory After Drug Administration
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Memory Improvement Confirmed with Zincure Drug, ZCS1
