A Review Paper Submitted To The Department Of Physiology School Of Medicine College Of Health Sciences And Addis Ababa University In Partial Fulfillment Of The Requirements For The Degree Of Master Of Science In Medical Physi

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized clinically byrnmemory and cognitive dysfunction and also protein misfolding-based rapid cognitive impairmentrnin the aging brain. It can inhibit the protein expression of specific genes by activating arnsequence-specific RNA degradation process. This is a powerful tool with which to study genernfunction, investigate the mechanism of the disease, and validate drug targets. In this review, wernsummarize the systems biology data on AD and pay particular attention to the proteomic changesrnin AD. Applying a systems biology model of the synapse, we attempt to integrate proteinrnchanges and provide an explanation of why seemingly diverse molecular changes result inrnmemory impairment. Finally, we give a systems biology model of AD explaining how AD canrndevelop in an individual manner in each particular subject but always results in a rapidlyrndeveloping dementia and memory impairment. Unfortunately, there is no effective therapeuticrnmethod for AD treatment or ways to halt disease progression. Many mechanisms are involved inrnthe disease, including genes mutation and protein dysfunction.rnKeywords: Alzheimer’s disease, Neurodegerative disease, Senile plaques, Assembled from β-rnamyloid (Aβ) peptides, & neurofibrillary tangles (NFT), Tau protein

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A Review Paper Submitted To The Department Of Physiology School Of Medicine College Of Health Sciences And Addis Ababa University In Partial Fulfillment Of The Requirements For The Degree Of Master Of Science In Medical Physi

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