Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
Tau-associated neuronal loss in the intermediate nucleus of the human hypothalamus, a putative VLPO analog, in progressive supranuclear palsy and Alzheimer's disease.
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Rastegar-Pouyani Shima, Lew Caroline, Pereira Felipe L, Satpati Abhijit, Arnas Ana Moreno, Paes Vitor, Leite Renata Elaine Paraízo, Suemoto Claudia Kimie, Spina Salvatore, Son Gowoon, Heinsen Helmut, Seeley William W, Walsh Christine M, Neylan Thomas C, Grinberg Lea T
Аннотация
BACKGROUND: Sleep phenotypes differ in progressive supranuclear palsy (PSP) and Alzheimer's disease (AD). The human intermediate nucleus (IntN), a putative ventrolateral preoptic analog, promotes non-rapid eye movement (NREM) sleep, but its disease-specific vulnerability is unclear.
METHODS: Post mortem hypothalami (n = 30; baseline [Braak stage I-II] n = 6; PSP n = 9; Braak III-IV n = 4; Braak V-VI n = 11) underwent marker-guided IntN delineation, galanin/phospho-tau (T231) immunohistochemistry, and stereology.
RESULTS: Advanced PSP showed profound IntN degeneration (84% neuron reduction vs baseline). In AD neuropathologic change, IntN neuronal loss and phospho-tau burden were greater in higher Braak stages and preferentially affected galanin-positive neurons (≈77% reduction in late AD); phospho-tau burden was higher in galanin-positive neurons.
CONCLUSIONS: The IntN is a disease-sensitive node, with near-ablation in PSP and progressive, preferential loss of detectable galaninergic neurons in AD. Although longitudinal observations and premortem sleep/wake measurements were not available for this sample, these findings are consistent with disease-level differences in NREM/ slow-wave sleep disturbance reported in PSP and AD.
METHODS: Post mortem hypothalami (n = 30; baseline [Braak stage I-II] n = 6; PSP n = 9; Braak III-IV n = 4; Braak V-VI n = 11) underwent marker-guided IntN delineation, galanin/phospho-tau (T231) immunohistochemistry, and stereology.
RESULTS: Advanced PSP showed profound IntN degeneration (84% neuron reduction vs baseline). In AD neuropathologic change, IntN neuronal loss and phospho-tau burden were greater in higher Braak stages and preferentially affected galanin-positive neurons (≈77% reduction in late AD); phospho-tau burden was higher in galanin-positive neurons.
CONCLUSIONS: The IntN is a disease-sensitive node, with near-ablation in PSP and progressive, preferential loss of detectable galaninergic neurons in AD. Although longitudinal observations and premortem sleep/wake measurements were not available for this sample, these findings are consistent with disease-level differences in NREM/ slow-wave sleep disturbance reported in PSP and AD.