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Nat Neurosci ; 26(4): 570-578, 2023 04.
Artigo em Inglês | MEDLINE | ID: mdl-36879142

RESUMO

There is a demand for noninvasive methods to ameliorate disease. We investigated whether 40-Hz flickering light entrains gamma oscillations and suppresses amyloid-ß in the brains of APP/PS1 and 5xFAD mouse models of Alzheimer's disease. We used multisite silicon probe recording in the visual cortex, entorhinal cortex or the hippocampus and found that 40-Hz flickering simulation did not engage native gamma oscillations in these regions. Additionally, spike responses in the hippocampus were weak, suggesting 40-Hz light does not effectively entrain deep structures. Mice avoided 40-Hz flickering light, associated with elevated cholinergic activity in the hippocampus. We found no reliable changes in plaque count or microglia morphology by either immunohistochemistry or in vivo two-photon imaging following 40-Hz stimulation, nor reduced levels of amyloid-ß 40/42. Thus, visual flicker stimulation may not be a viable mechanism for modulating activity in deep structures.


Assuntos
Doença de Alzheimer , Camundongos , Animais , Peptídeos beta-Amiloides/metabolismo , Encéfalo/metabolismo , Hipocampo/metabolismo , Microglia/metabolismo , Camundongos Transgênicos , Modelos Animais de Doenças , Precursor de Proteína beta-Amiloide , Placa Amiloide
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