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Erica Sequeira and N.Saraswathy*


Alzheimer’s disease is the most common form of dementia. It is a progressive and irreversible neurodegenerative disorder and characterized clinically by progressive loss of memory, cognition, reasoning, judgment and emotional stability. The brains of people with Alzheimer’s disease have two abnormal structures such as the senile plaques containing amyloid β and the neurofibrillary tangles containing Tau, which are the hallmarks of the disease. Over time, this damage spreads to other areas of the brain, such as the grey matter (responsible for processing thoughts) and the hippocampus (responsible for memory).This results in decline in the neuronal mass and cognitive functions. The actual pathogenesis of Alzheimer's disease is thought to begin many years before the diagnosis of Alzheimer’s disease. Thus such a long "preclinical" phase of Alzheimer’s disease would provide a critical opportunity for therapeutic intervention and prevent the disease in future. These amyloid plaques are formed due to the proteolytic cleavage of amyloid precursor protein (APP) by β-secretase and γ-secretase. This article reviews on the secretases, that are responsible for the pathogenesis of Alzheimer’s disease, molecular explanation of the possible neuropathogenesis, the cleavage products generated by different processing patterns and the potential role of those cleavage products.

Keywords: Alzheimer’s disease, amyloid, neurofibrillary tangles, APP, ?-secretase, ?- secretase, ?-secretase, oxidative stress.

[Full Text Article]

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