Your browser doesn't support javascript.
loading
Circadian and sleep dysfunction in Alzheimer's disease.
Uddin, Md Sahab; Tewari, Devesh; Mamun, Abdullah Al; Kabir, Md Tanvir; Niaz, Kamal; Wahed, Mir Imam Ibne; Barreto, George E; Ashraf, Ghulam Md.
Afiliación
  • Uddin MS; Department of Pharmacy, Southeast University, Dhaka, Bangladesh; Pharmakon Neuroscience Research Network, Dhaka, Bangladesh. Electronic address: msu-neuropharma@hotmail.com.
  • Tewari D; Department of Pharmacognosy, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab, India.
  • Mamun AA; Department of Pharmacy, Southeast University, Dhaka, Bangladesh; Pharmakon Neuroscience Research Network, Dhaka, Bangladesh.
  • Kabir MT; Department of Pharmacy, BRAC University, Dhaka, Bangladesh.
  • Niaz K; Department of Pharmacology and Toxicology, Faculty of Bioscience and Agri-Food and Environmental Technology, University of Teramo, 64100, Italy.
  • Wahed MII; Department of Pharmacy, University of Rajshahi, Rajshahi, Bangladesh.
  • Barreto GE; Department of Biological Sciences, University of Limerick, Limerick, Ireland; Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile. Electronic address: George.Barreto@ul.ie.
  • Ashraf GM; King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia. Electronic address: gashraf@kau.edu.sa.
Ageing Res Rev ; 60: 101046, 2020 07.
Article en En | MEDLINE | ID: mdl-32171783
Alzheimer's disease (AD) is a devastating and irreversible cognitive impairment and the most common type of dementia. Along with progressive cognitive impairment, dysfunction of the circadian rhythms also plays a pivotal role in the progression of AD. A mutual relationship among circadian rhythms, sleep, and AD has been well-recommended. The etiopathogenesis of the disturbances of the circadian system and AD share some general features that also unlock the outlook of observing them as a mutually dependent pathway. Indeed, the burden of amyloid ß (Aß), neurofibrillary tangles (NFTs), neuroinflammation, oxidative stress, and dysfunction of circadian rhythms may lead to AD. Aging can alter both sleep timings and quality that can be strongly disrupted in AD. Increased production of Aß and reduced Aß clearance are caused by a close interplay of Aß, sleep disturbance and raised wakefulness. Besides Aß, the impact of tau pathology is possibly noteworthy to the sleep deprivation found in AD. Hence, this review is focused on the primary mechanistic complexities linked to disruption of circadian rhythms, sleep deprivation, and AD. Furthermore, this review also highlights the potential therapeutic strategies to abate AD pathogenesis.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trastornos del Sueño-Vigilia / Enfermedad de Alzheimer Límite: Humans Idioma: En Revista: Ageing Res Rev Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trastornos del Sueño-Vigilia / Enfermedad de Alzheimer Límite: Humans Idioma: En Revista: Ageing Res Rev Asunto de la revista: GERIATRIA Año: 2020 Tipo del documento: Article Pais de publicación: Reino Unido