Abstract
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.
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This post is Copyright: | September 9, 2026
Neuro-Dementia