proteinopathy-induced neuronal senescence a hypothesis for brain failure in alzheimers and other neurodegenerative diseasesproteinopathy-induced神经元衰老大脑失败的假设老年痴呆症和其他神经退行性疾病.pdfVIP

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proteinopathy-induced neuronal senescence a hypothesis for brain failure in alzheimers and other neurodegenerative diseasesproteinopathy-induced神经元衰老大脑失败的假设老年痴呆症和其他神经退行性疾病.pdf

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proteinopathy-induced neuronal senescence a hypothesis for brain failure in alzheimers and other neurodegenerative diseasesproteinopathy-induced神经元衰老大脑失败的假设老年痴呆症和其他神经退行性疾病

Available online /content/1/2/5 Review Proteinopathy-induced neuronal senescence: a hypothesis for brain failure in Alzheimer’s and other neurodegenerative diseases Todd E Golde and Victor M Miller 1Department of Neuroscience, Mayo Clinic, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, Florida 32224, USA Corresponding author: Todd E Golde, tgolde@ Published: 13 October 2009 Alzheimer’s Research Therapy 2009, 1:5 (doi:10.1186/alzrt5) This article is online at /content/1/2/5 © 2009 BioMed Central Ltd Genetic, pathological, biochemical, animal and cell modeling Abstract studies provide strong support for the general hypothesis that Background: Alzheimer’s disease (AD) and a host of other accumulation of misfolded, aggregated proteins in the brain neurodegenerative central nervous system (CNS) proteinopathies triggers a complex series of events that result in neuronal are characterized by the accumulation of misfolded protein aggre- degeneration [1-4]. In Alzheimer’s disease (AD) aggregation gates. Simplistically, these aggregates can be divided into and accumulation of the amyloid β (Aβ) protein and smaller, soluble, oligomeric and larger, less-soluble or insoluble, microtubule associated protein tau (MAPT) have both been fibrillar forms. Perhaps the major ongoing debate in the implicated as key pathogenic ‘triggers’ [5]. Aβ accumulates in neurodegenerative disease field is whether the smaller oligomeric or larger fibrillar aggregates are the primary neurotoxin. Herein, we senile plaques, cerebral vessels, and, to a more lim