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Neuronal and glial vulnerability of the suprachiasmatic nucleus in tauopathies: evidence from human studies and animal models.
Son, Gowoon; Neylan, Thomas C; Grinberg, Lea T.
Afiliación
  • Son G; Memory and Aging Center, Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, San Francisco, CA, USA.
  • Neylan TC; Memory and Aging Center, Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, San Francisco, CA, USA.
  • Grinberg LT; Department of Psychiatry, University of California, San Francisco, San Francisco, CA, USA.
Mol Neurodegener ; 19(1): 4, 2024 Jan 10.
Article en En | MEDLINE | ID: mdl-38195580
ABSTRACT
Tauopathies, a group of neurodegenerative diseases that includes Alzheimer's disease, commonly lead to disturbances in sleep-wake patterns and circadian rhythm disorders. The circadian rhythm, a recurring 24-hour cycle governing human biological activity, is regulated by the hypothalamic suprachiasmatic nucleus (SCN) and endogenous transcriptional-translational feedback loops. Surprisingly, little attention has been given to investigating tauopathy-driven neuropathology in the SCN and the repercussions of SCN and circadian gene dysfunction in the human brain affected by tauopathies. This review aims to provide an overview of the current literature on the vulnerability of the SCN in tauopathies in humans. Emphasis is placed on elucidating the neuronal and glial changes contributing to the widespread disruption of the molecular circadian clock. Furthermore, this review identifies areas of knowledge requiring further investigation.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Tauopatías / Enfermedad de Alzheimer Límite: Animals / Humans Idioma: En Revista: Mol Neurodegener Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Tauopatías / Enfermedad de Alzheimer Límite: Animals / Humans Idioma: En Revista: Mol Neurodegener Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos