{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T00:10:00Z","timestamp":1790122200001,"version":"4.0.1"},"reference-count":427,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2024,4,16]],"date-time":"2024-04-16T00:00:00Z","timestamp":1713225600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2024,4,16]]},"abstract":"<jats:p>The \u201camyloid cascade\u201d hypothesis of Alzheimer\u2019s disease (AD) pathogenesis invokes the accumulation in the brain of plaques (containing the amyloid-\u03b2 protein precursor [A\u03b2PP] cleavage product amyloid-\u03b2 [A\u03b2]) and tangles (containing hyperphosphorylated tau) as drivers of pathogenesis. However, the poor track record of clinical trials based on this hypothesis suggests that the accumulation of these peptides is not the only cause of AD. Here, an alternative hypothesis is proposed in which the A\u03b2PP cleavage product C99, not A\u03b2, is the main culprit, via its role as a regulator of cholesterol metabolism. C99, which is a cholesterol sensor, promotes the formation of mitochondria-associated endoplasmic reticulum (ER) membranes (MAM), a cholesterol-rich lipid raft-like subdomain of the ER that communicates, both physically and biochemically, with mitochondria. We propose that in early-onset AD (EOAD), MAM-localized C99 is elevated above normal levels, resulting in increased transport of cholesterol from the plasma membrane to membranes of intracellular organelles, such as ER\/endosomes, thereby upregulating MAM function and driving pathology. By the same token, late-onset AD (LOAD) is triggered by any genetic variant that increases the accumulation of intracellular cholesterol that, in turn, boosts the levels of C99 and again upregulates MAM function. Thus, the functional cause of AD is upregulated MAM function that, in turn, causes the hallmark disease phenotypes, including the plaques and tangles. Accordingly, the MAM hypothesis invokes two key interrelated elements, C99 and cholesterol, that converge at the MAM to drive AD pathogenesis. From this perspective, AD is, at bottom, a lipid disorder.<\/jats:p>","DOI":"10.3233\/jad-231318","type":"journal-article","created":{"date-parts":[[2024,4,5]],"date-time":"2024-04-05T11:48:24Z","timestamp":1712317704000},"page":"1243-1275","source":"Crossref","is-referenced-by-count":12,"title":["Towards a Unitary Hypothesis of Alzheimer\u2019s Disease Pathogenesis"],"prefix":"10.1177","volume":"98","author":[{"given":"Estela","family":"Area-Gomez","sequence":"first","affiliation":[{"name":"Department of Neurology, Columbia University, New York, NY, USA"},{"name":"Centro de Investigaciones Biol\u00f3gicas \u201cMargarita Salas\u201d, Spanish National Research Council, Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric A.","family":"Schon","sequence":"additional","affiliation":[{"name":"Department of Neurology, Columbia University, New York, NY, USA"},{"name":"Department of Genetics and Development>, Columbia University, New York, NY, 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