{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T20:02:43Z","timestamp":1791489763910,"version":"4.3.4"},"reference-count":75,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,12,26]],"date-time":"2025-12-26T00:00:00Z","timestamp":1766707200000},"content-version":"vor","delay-in-days":25,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T00:00:00Z","timestamp":1764547200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100001797","name":"Pharmaceutical Research and Manufacturers of America Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001797","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008918","name":"Jean Perkins Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008918","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp; Dementia"],"published-print":{"date-parts":[[2025,12]]},"abstract":"Abstract<\/jats:title>\n \n INTRODUCTION<\/jats:title>\n Synaptic spine loss in Alzheimer's disease (AD) contributes to cognitive decline. p21\u2010activated kinase 1 (PAK1), a regulator of spine integrity, is aberrantly activated in AD. We investigated whether PAK1 inhibition might preserve dendritic spines in vitro and in vivo.<\/jats:p>\n <\/jats:sec>\n \n METHODS<\/jats:title>\n Oligomeric amyloid beta (oA\u03b2) or tau (oTau) were applied to hippocampal neurons\u00a0\u00b1 NVS\u2010PAK1\u20101, a selective PAK1 inhibitor. NVS\u2010PAK1\u20101 was orally administered to 5xFAD mice. The effects of NVS\u2010PAK1\u20101 treatment on PAK1 activity, spine density, and the proteome were assessed using phospho\u2010PAK1 (pPAK1) western blotting, Golgi staining, and mass spectrometry for proteomic analyses.<\/jats:p>\n <\/jats:sec>\n \n RESULTS<\/jats:title>\n NVS\u2010PAK1\u20101 prevented oA\u03b2 and oTau\u2013induced spine loss in vitro. In 5xFAD mice, NVS\u2010PAK1\u20101 demonstrated brain exposure after oral administration and reduced PAK1 activation, prevented spine loss, and partially normalized synaptic proteomic signatures in females in absence of alterations in brain or plasma A\u03b2.<\/jats:p>\n <\/jats:sec>\n \n DISCUSSION<\/jats:title>\n PAK1 inhibition enhances spine resilience in AD models, supporting its therapeutic potential.<\/jats:p>\n <\/jats:sec>\n \n Highlights<\/jats:title>\n \n \n \n p21\u2010activated kinase 1 (PAK1) inhibitors prevent oligomeric amyloid beta (oA\u03b2) and oligomeric tau\u2013induced spine loss and dendritic degeneration in cultured mouse hippocampal neurons.<\/jats:p>\n <\/jats:list-item>\n \n \n NVS\u2010PAK1\u20101, a selective PAK1 inhibitor, protects against oA\u03b2\u2010induced spine loss in a dose\u2010dependent manner (EC\n 50<\/jats:sub>\n \u00a0=\u00a02\u00a0nM).\n <\/jats:p>\n <\/jats:list-item>\n \n Oral administration of NVS\u2010PAK1\u20101 achieves brain penetration and bioavailability in normal CD\u20101 mice, and target engagement in 5xFAD mice.<\/jats:p>\n <\/jats:list-item>\n \n Chronic NVS\u2010PAK1\u20101 treatment mitigates spine loss in the somatosensory cortex of 6\u2010month\u2010old 5xFAD female mice.<\/jats:p>\n <\/jats:list-item>\n \n Chronic treatment with NVS\u2010PAK1\u20101 restores proteomic abundance of actin cytoskeleton and dendritic spine\u2010associated proteins, including cofilin 2 and pyruvate dehydrogenase kinases, downstream of PAK1 in young 5xFAD female mice showing spine resilience.<\/jats:p>\n <\/jats:list-item>\n \n Clinical oncology trials with other PAK1 inhibitors support potential repurposing or novel compound development for Alzheimer's disease trials.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n 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