This review aims to summarize how Tau pathology, in particular, brings about Alzheimer’s disease (AD). Various studies from the past decade have been analyzed with the purpose of providing a compact descrip-tion on h...This review aims to summarize how Tau pathology, in particular, brings about Alzheimer’s disease (AD). Various studies from the past decade have been analyzed with the purpose of providing a compact descrip-tion on how Tau protein infl uences AD. The pathologies associated with the accumulation of Amyloid and Tau have always been at the forefront of all research on Alzheimer’s disease, which have usually centered around a deeper understanding of the pathophysiological mechanisms, or on developing therapeutics targeting these proteins. Recent data has also continuously been challenging the ubiquitous acceptance of amyloid being the driving force for Alzheimer’s disease as anamyloid therapies continue to fail. Tau protein shows an independent ability to accumulate within nerve cells, and its propagation shows a continuous seeding and spreading patiern. The purpose of this review is thus to enforce the importance of Tau pathology and tailor future developments in AD treatment accordingly. By the end of this review, we thus infer how regional accumulations of Tau aff ect AD, how and why the amyloid cascade hypothesis needs to change, and we end by looking at fi ndings from the recent “Beyond Amyloid” symposium where factors like a loss in DNA integrity, cell cycle disorders and microtubular dysregulation have been proposed as potential mediators of AD.展开更多
文摘This review aims to summarize how Tau pathology, in particular, brings about Alzheimer’s disease (AD). Various studies from the past decade have been analyzed with the purpose of providing a compact descrip-tion on how Tau protein infl uences AD. The pathologies associated with the accumulation of Amyloid and Tau have always been at the forefront of all research on Alzheimer’s disease, which have usually centered around a deeper understanding of the pathophysiological mechanisms, or on developing therapeutics targeting these proteins. Recent data has also continuously been challenging the ubiquitous acceptance of amyloid being the driving force for Alzheimer’s disease as anamyloid therapies continue to fail. Tau protein shows an independent ability to accumulate within nerve cells, and its propagation shows a continuous seeding and spreading patiern. The purpose of this review is thus to enforce the importance of Tau pathology and tailor future developments in AD treatment accordingly. By the end of this review, we thus infer how regional accumulations of Tau aff ect AD, how and why the amyloid cascade hypothesis needs to change, and we end by looking at fi ndings from the recent “Beyond Amyloid” symposium where factors like a loss in DNA integrity, cell cycle disorders and microtubular dysregulation have been proposed as potential mediators of AD.
