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Unlike mice, aging macaques have extensive association cortices and inflammatory signaling similar to humans, are apolipoprotein E \u03b54 homozygotes, and naturally develop tau and amyloid pathology with marked cognitive deficits. Importantly, monkeys provide the unique opportunity to study early\u2010stage, soluble hyperphosphorylated tau (p\u2010tau), including p\u2010tau217. As soluble p\u2010tau is rapidly dephosphorylated\n                      <jats:italic>post mortem<\/jats:italic>\n                      , it is not captured in human brains except with biopsy material. However, new macaque data show that soluble p\u2010tau is toxic to neurons and capable of seeding across cortical circuits. Extensive evidence indicates that age\u2010related inflammatory signaling contributes to calcium dysregulation, which drives tau hyperphosphorylation and amyloid beta generation. Pharmacological studies in aged macaques suggest that inhibiting inflammation and restoring calcium regulation can reduce tau hyperphosphorylation with minimal side effects, appropriate for potential preventive therapeutics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Aging monkeys provide a unique window into early stage, soluble phosphorylated tau (p\u2010tau).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Inflammation with advancing age leads to calcium dysregulation, p\u2010tau, and amyloid beta (A\u03b2).<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Macaque research shows p\u2010tau undergoes transsynaptic seeding early in the cortex.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>p\u2010tau traps amyloid precursor protein\u2013containing endosomes, which may increase A\u03b2 and drive vicious cycles.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Restoring calcium regulation in cortex reduced p\u2010tau217 levels in aged macaques.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.14477","type":"journal-article","created":{"date-parts":[[2025,1,8]],"date-time":"2025-01-08T09:14:28Z","timestamp":1736327668000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["The etiology and prevention of early\u2010stage tau pathology in higher cortical circuits: Insights from aging rhesus macaques"],"prefix":"10.1002","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5415-3067","authenticated-orcid":false,"given":"Dibyadeep","family":"Datta","sequence":"first","affiliation":[{"name":"Department of Psychiatry Yale Medical School  New Haven Connecticut USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy F. 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