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Epigenetics and Late-Onset Alzheimer’s Disease

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Epigenetic Aspects of Chronic Diseases

Abstract

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease, affecting about 20 million people worldwide.35 It is characterized by progressive loss of memory, declining cognitive function and, ultimately, leads to decreasing physical functions and death. The neuropathological hallmarks of AD are the development of senile plaques and the formation of neurofibrillary tangles, intracellular neuronal lesions deposited in the brain. The neurofibrillary tangles represent bundles of paired helical filaments, which mainly consist of the microtubule-associated protein tau in an abnormally phosphorylated form.2 The extracellular amyloid plaques mainly consist of the 42-residue long amyloid β-peptide which is proteolytically derived from the much larger amyloid precursor protein (APP).27 The generation and subsequent aggregation of amyloid beta (Aβ) seems to be at the origin of the disease and is believed to trigger a complex pathological cascade that ultimately causes neuronal dysfunction.

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Schumacher, A., Bihaqi, S., Zawia, N.H. (2011). Epigenetics and Late-Onset Alzheimer’s Disease. In: Roach, H., Bronner, F., Oreffo, R. (eds) Epigenetic Aspects of Chronic Diseases. Springer, London. https://doi.org/10.1007/978-1-84882-644-1_12

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