Rappoport Ari
The Rachel and Selim Benin School of Computer Science and Engineering, The Hebrew University of Jerusalem, Jerusalem, Israel; email:
Annu Rev Biochem. 2025 Jun;94(1):387-416. doi: 10.1146/annurev-biochem-052024-115455. Epub 2024 Oct 30.
I present a theory of Alzheimer's disease (AD) that explains its symptoms, pathology, and risk factors. To do this, I introduce a new theory of brain plasticity that elucidates the physiological roles of AD-related agents. New events generate synaptic and branching candidates competing for long-term enhancement. Competition resolution crucially depends on the formation of membrane lipid rafts, which requires astrocyte-produced cholesterol. Sporadic AD is caused by impaired formation of plasma-membrane lipid rafts, preventing the conversion of short- to long-term memory and yielding excessive tau phosphorylation, intracellular cholesterol accumulation, synaptic dysfunction, and neurodegeneration. Amyloid β (Aβ) production is promoted by cholesterol during the switch to competition resolution, and cholesterol accumulation stimulates chronic Aβ production, secretion, and aggregation. The theory addresses all of the major established facts known about the disease and is supported by strong evidence.
我提出了一种阿尔茨海默病(AD)理论,该理论解释了其症状、病理和风险因素。为此,我引入了一种新的脑可塑性理论,阐明了与AD相关因子的生理作用。新事件会产生竞争长期增强的突触和分支候选物。竞争的解决关键取决于膜脂筏的形成,而这需要星形胶质细胞产生的胆固醇。散发性AD是由质膜脂筏形成受损引起的,这会阻止短期记忆向长期记忆的转化,并导致过度的tau蛋白磷酸化、细胞内胆固醇积累、突触功能障碍和神经退行性变。在向竞争解决转变的过程中,胆固醇会促进淀粉样β(Aβ)的产生,而胆固醇积累会刺激慢性Aβ的产生、分泌和聚集。该理论涵盖了关于该疾病的所有主要既定事实,并得到了有力证据的支持。