{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T17:28:29Z","timestamp":1792171709956,"version":"4.4.0"},"posted":{"date-parts":[[2024,3,12]]},"group-title":"Neuroscience","reference-count":70,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,5,20]]},"abstract":"<jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>\n                    Sleep-wake dysfunction is an early and common event in Alzheimer\u2019s disease (AD). The lateral hypothalamic area (LHA) regulates the sleep and wake cycle through wake-promoting orexinergic neurons (Orx\n                    <jats:sup>N<\/jats:sup>\n                    ) and sleep-promoting melanin-concentrating hormone or MCHergic neurons (MCH\n                    <jats:sup>N<\/jats:sup>\n                    ). These neurons share close anatomical proximity with functional reciprocity. This study investigated LHA Orx\n                    <jats:sup>N<\/jats:sup>\n                    and MCH\n                    <jats:sup>N<\/jats:sup>\n                    loss patterns in AD individuals. Understanding the degeneration pattern of these neurons will be instrumental in designing potential therapeutics to slow down the disease progression and remediate the sleep-wake dysfunction in AD.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    Postmortem human brain tissue from donors with AD (across progressive stages) and controls were examined using unbiased stereology. Formalin-fixed, celloidin-embedded hypothalamic sections were stained with Orx-A\/MCH, p-tau (CP13), and counterstained with gallocyanin. Orx or MCH-positive neurons with or without CP13 inclusions and gallocyanin-stained neurons were considered for stereology counting. Additionally, we extracted RNA from the LHA using conventional techniques. We used customized Neuropathology and Glia nCounter\n                    <jats:sup>\u00ae<\/jats:sup>\n                    (Nanostring) panels to study gene expression. Wald statistical test was used to compare the groups, and the genes were considered differentially expressed when the p-value was &lt;.05.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    We observed a progressive decline in Orx\n                    <jats:sup>N<\/jats:sup>\n                    alongside a relative preservation of MCH\n                    <jats:sup>N<\/jats:sup>\n                    . Orx\n                    <jats:sup>N<\/jats:sup>\n                    decreased by 58% (p=.03) by Braak stages (BB) 1-2 and further declined to 81% (p=.03) by BB 5-6. Conversely, MCH\n                    <jats:sup>N<\/jats:sup>\n                    demonstrated a non-statistical significant decline (27%, p=.1088) by BB 6. We observed a progressive increase in differentially expressed genes (DEGs), starting with glial profile changes in BB2. While Orx\n                    <jats:sup>N<\/jats:sup>\n                    loss was observed, Orx-related genes showed upregulation in BB 3-4 compared to BB 0-1. GO and KEGG terms related to neuroinflammatory pathways were mainly enriched.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>\n                    To date, Orx\n                    <jats:sup>N<\/jats:sup>\n                    loss in the LHA represents the first neuronal population to die preceding the loss of LC neurons. Conversely, MCHN shows resilience to AD p-tau accumulation across Braak stages. The initial loss of Orx\n                    <jats:sup>N<\/jats:sup>\n                    correlates with specific neuroinflammation, glial profile changes, and overexpression of HCRT, possibly due to hyperexcitation following compensation mechanisms. Interventions preventing Orx\n                    <jats:sup>N<\/jats:sup>\n                    loss and inhibiting p-tau accumulation in the LHA could prevent neuronal loss in AD and, perhaps, the progression of the disease.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.1101\/2024.03.06.583765","type":"posted-content","created":{"date-parts":[[2024,3,12]],"date-time":"2024-03-12T14:05:12Z","timestamp":1710252312000},"source":"Crossref","is-referenced-by-count":6,"title":["The wake- and sleep-modulating neurons of the lateral hypothalamic area demonstrate a differential pattern of degeneration in Alzheimer\u2019s disease"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2674-7973","authenticated-orcid":false,"given":"Abhijit","family":"Satpati","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felipe L.","family":"Pereira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander V.","family":"Soloviev","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mihovil","family":"Mladinov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Larsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Song Hua","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chia-Ling","family":"Tu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata E. 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