{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T19:05:52Z","timestamp":1777489552240,"version":"3.51.4"},"reference-count":81,"publisher":"SAGE Publications","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2023,12,6]]},"abstract":"<jats:p>Background: Emerging evidence has revealed that dysregulation of the hormone ghrelin and its receptor, growth hormone secretagogue receptor (GHSR), contributes to the pathogenesis of Alzheimer\u2019s disease (AD). Specifically, defective GHSR function and resultant hippocampal ghrelin resistance are linked to hippocampal synaptic injury in AD paradigms. Also, AD patients exhibit elevated ghrelin activation. However, the detailed molecular mechanisms of hippocampal GHSR dysfunction and the relevance of ghrelin elevation to hippocampal ghrelin resistance in AD-relevant pathological settings are not fully understood. Objective: In the current study, we employed a recently established mouse line of AD risk [humanized amyloid beta knockin (hA\u03b2 KI mice), also referred to as a mouse model of late-onset AD in previous literature] to further define the role of ghrelin system dysregulation in the development of AD. Methods: We employed multidisciplinary techniques to determine the change of plasma ghrelin and the functional status of GHSR in hA\u03b2 KI mice as well as primary neuron cultures. Results: We observed concurrent plasma ghrelin elevation and hippocampal GHSR desensitization with disease progression. Further examination excluded the possibility that ghrelin elevation is a compensatory change in response to GHSR dysfunction. In contrast, further in vitro and in vivo results show that agonist-mediated overstimulation potentiates GHSR desensitization through enhanced GHSR internalization. Conclusions: These findings suggest that circulating ghrelin elevation is a pathological event underlying hippocampal GHSR dysfunction, culminating in hippocampal ghrelin resistance and resultant synaptic injury in late-onset AD-related settings.<\/jats:p>","DOI":"10.3233\/jad-231002","type":"journal-article","created":{"date-parts":[[2023,11,21]],"date-time":"2023-11-21T11:34:05Z","timestamp":1700566445000},"page":"1579-1592","source":"Crossref","is-referenced-by-count":3,"title":["Elevated Ghrelin Promotes Hippocampal Ghrelin Receptor Defects in Humanized Amyloid-\u03b2 Knockin Mice During Aging"],"prefix":"10.1177","volume":"96","author":[{"given":"Jing","family":"Tian","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"},{"name":"Blue Valley West High School, Overland Park, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kun","family":"Jia","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tienju","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lan","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey M.","family":"Zigman","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Center for Hypothalamic Research, The University of Texas Southwestern Medical Center, Dallas, TX, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Heng","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, The University of Kansas, Lawrence, KS, USA"},{"name":"Alzheimer\u2019s disease Research Center (ADRC), Department of Neurology, The University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-231002_ref1","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1186\/s13024-019-0333-5","article-title":"The neuropathological diagnosis of Alzheimer\u2019s disease","volume":"14","author":"DeTure","year":"2019","journal-title":"Mol Neurodegener"},{"key":"10.3233\/JAD-231002_ref2","doi-asserted-by":"crossref","first-page":"19","DOI":"10.1038\/s41582-022-00749-z","article-title":"Synaptic degeneration in Alzheimer 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