{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:50:54Z","timestamp":1791273054735,"version":"4.1.0"},"reference-count":64,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:00:00Z","timestamp":1791158400000},"content-version":"vor","delay-in-days":4,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100016005","name":"Yulgilbar Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100016005","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008710","name":"Dementia Australia Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008710","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Heat shock protein 72 (Hsp72), a stress\u2010inducible member of the Hsp70 family, has been implicated in mitigating the pathogenic effects of amyloid\u2010beta (A\u03b2) and tau pathology; both key factors associated with the development and progression of Alzheimer's disease (AD). However, no in\u00a0vivo study has been conducted to investigate the ability of Hsp72 to provide benefit when both A\u03b2 and tau pathology are present concurrently. This study set out to utilize a genetic approach (transgenic overexpression) and a pharmacological validation approach (BGP\u201015) to increase Hsp72 expression in mice exhibiting A\u03b2 and tau pathology (5xFADxTg30 model). Our findings indicate that genetic Hsp72 overexpression did not significantly alter A\u03b2 or tau burden, deficits in motor performance, or alterations to body composition in this model, but modestly improved survival rates (driven by findings in male mice) and altered anxiety\u2010like behavior (driven by findings in female mice). Similarly, BGP\u201015 treatment was unable to rescue behavioral traits, motor deficits, body composition, or alleviate A\u03b2 or tau accumulation, although this treatment also showed a trend towards enhancing survival (again in male mice) and altered anxiety\u2010like behavior (specifically in female mice). While the 5xFADxTg30 mice demonstrated seizure susceptibility compared to WT mice, BGP\u201015 was unable to alleviate this trait. These findings were independent of any measurable increase in Hsp72 abundance in the brain in response to BGP\u201015. Together, these findings suggest a limited impact of genetic overexpression and pharmacological targeting of Hsp72 protein abundance in this combined A\u03b2 and tau model, although some sex\u2010specific differences are noted.<\/jats:p>","DOI":"10.1002\/jnr.70161","type":"journal-article","created":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T06:54:48Z","timestamp":1791269688000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genetic and Pharmacological Targeting of Hsp72 Overexpression\/Induction in an Alzheimer's Disease Mouse Model With Combined Amyloid and Tau Pathology"],"prefix":"10.1002","volume":"104","author":[{"given":"J. P. S.","family":"Marshall","sequence":"first","affiliation":[{"name":"Baker Heart and Diabetes Institute  Melbourne Australia"},{"name":"School of Medicine, Dentistry and Health Sciences The University of Melbourne  Melbourne Australia"},{"name":"The Florey Institute of Neuroscience and Mental Health  Melbourne Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6165-5639","authenticated-orcid":false,"given":"A.","family":"Harutyunyan","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, School of Translational Medicine Monash University  Melbourne Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-6675-7490","authenticated-orcid":false,"given":"J.","family":"Ng","sequence":"additional","affiliation":[{"name":"School of Health Sciences The University of Tasmania  Launceston Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"O. 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E.","family":"King","sequence":"additional","affiliation":[{"name":"Wicking Dementia Research and Education Centre, UTAS Health University of Tasmania  Hobart Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Morizzi","sequence":"additional","affiliation":[{"name":"Monash Institute of Pharmaceutical Sciences  Melbourne Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Wright","sequence":"additional","affiliation":[{"name":"Monash Institute of Pharmaceutical Sciences  Melbourne Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. C.","family":"Calkin","sequence":"additional","affiliation":[{"name":"Baker Heart and Diabetes Institute  Melbourne Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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