{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T07:48:26Z","timestamp":1791877706072,"version":"4.3.4"},"reference-count":434,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2023,6,13]],"date-time":"2023-06-13T00:00:00Z","timestamp":1686614400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>The enormous, 2\u20133-million-year evolutionary expansion of hominin neocortices to the current enormity enabled humans to take over the planet. However, there appears to have been a glitch, and it occurred without a compensatory expansion of the entorhinal cortical (EC) gateway to the hippocampal memory-encoding system needed to manage the processing of the increasing volume of neocortical data converging on it. The resulting age-dependent connectopathic glitch was unnoticed by the early short-lived populations. It has now surfaced as Alzheimer\u2019s disease (AD) in today\u2019s long-lived populations. With advancing age, processing of the converging neocortical data by the neurons of the relatively small lateral entorhinal cortex (LEC) inflicts persistent strain and high energy costs on these cells. This may result in their hyper-release of harmless A\u03b21\u201342 monomers into the interstitial fluid, where they seed the formation of toxic amyloid-\u03b2 oligomers (A\u03b2Os) that initiate AD. At the core of connectopathic AD are the postsynaptic cellular prion protein (PrPC). Electrostatic binding of the negatively charged A\u03b2Os to the positively charged N-terminus of PrPC induces hyperphosphorylation of tau that destroys synapses. The spread of these accumulating A\u03b2Os from ground zero is supported by A\u03b2\u2019s own production mediated by target cells\u2019 Ca2+-sensing receptors (CaSRs). These data suggest that an early administration of a strongly positively charged, A\u03b2Os-interacting peptide or protein, plus an inhibitor of CaSR, might be an effective AD-arresting therapeutic combination.<\/jats:p>","DOI":"10.3390\/cells12121618","type":"journal-article","created":{"date-parts":[[2023,6,14]],"date-time":"2023-06-14T01:32:15Z","timestamp":1686706335000},"page":"1618","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Alzheimer\u2019s Disease and Its Possible Evolutionary Origin: Hypothesis"],"prefix":"10.3390","volume":"12","author":[{"given":"James F.","family":"Whitfield","sequence":"first","affiliation":[{"name":"Human Health Therapeutics, National Research Council, Ottawa, ON K1A 0R6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kerry","family":"Rennie","sequence":"additional","affiliation":[{"name":"Human Health Therapeutics, National Research Council, Ottawa, ON K1A 0R6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balu","family":"Chakravarthy","sequence":"additional","affiliation":[{"name":"Human Health Therapeutics, National Research Council, Ottawa, ON K1A 0R6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,6,13]]},"reference":[{"key":"ref_1","unstructured":"Kraepelin, E. 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