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Updated: Feb 26, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

運動と運動関連傷害の影響：βアミロイドおよびβアミロイド前駆体タンパク質の合成と処理

Weizhe Zhen¹, Yanfeng Xing², Yongqin Li²

¹Graduate School, Capital Medical University, Beijing, China.

Frontiers in cellular neuroscience

|February 25, 2026

Abstract:

During the processing and assembly of β-amyloid precursor protein (APP), the amyloidogenic pathway represents a crucial component of Alzheimer's disease (AD) pathogenesis. The non-amyloidogenic pathway does not generate toxic Aβ. For a long time, research has delved deeply into both pathways, elucidating numerous important details and mechanisms within these processes. Scientists and clinicians have sought to design effective therapeutic interventions based on these mechanisms. However, this endeavor has encountered numerous setbacks, resulting in no currently available drugs capable of reversing AD progression. Regarding APP processing and assembly, we are curious whether daily activities influence these processes. We focus on exercise as a daily activity, systematically exploring whether it affects APP processing and assembly and the underlying mechanisms. Furthermore, we examine alterations in APP processing and assembly in exercise-related injury disorders, summarizing and analyzing existing research. We discuss promising future research directions, aiming to contribute to preventing adverse outcomes following exercise-related injuries.

キーワード:

運動運動関連傷害処理合成 βアミロイド βアミロイド前駆体タンパク質

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Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

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Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...

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