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The aggregation propensity of Tau and amyloid-β in Alzheimer's disease
Subashchandrabose Chinnathambi1, Murugappan Kumarappan1, Madhura Chandrashekar1
1Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Institute of National Importance, Hosur Road, Bangalore, Karnataka, India.
Abstract:
Alzheimer disease is a multifactorial disease and can be due to many factors which includes gene mutation, cellular stress, toxicity, neuroinflammation, biomolecules dyshomeostasis, organelle stress and dysfunction, age, gender, ethnicity and other medical conditions are correlate with AD. Alzheimer disease, a progressive neurodegenerative disease characterized by presence of amyloid plaques and neurofibrillary tangles. These protein aggregates cause neurodegeneration, leading to cognition decline, finally memory loss. During disease progression, cross talk between the factors one with each other making disease condition worsen. Cross-talk leads to several cellular changes mainly functional change in both neural and neuro-glial cells. The neuronal changes are mitochondrial dysfunction, endoplasmic reticulum stress and synaptic loss. The neuro-glial changes include demyelination, neuroinflammation and phagocytosis. This change releases few proteins in CSF and blood which can be used as biomarker.
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