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{
  "pmid": "28611660",
  "doi": "10.3389/fnagi.2017.00170",
  "abstract": "1. Front Aging Neurosci. 2017 May 30;9:170. doi: 10.3389/fnagi.2017.00170. \neCollection 2017.\n\nNeurodegeneration and the Circadian Clock.\n\nHood S(1), Amir S(2).\n\nAuthor information:\n(1)Department of Psychology, Bishop's UniversitySherbrooke, QC, Canada.\n(2)Department of Psychology, Concordia UniversityMontreal, QC, Canada.\n\nDespite varied etiologies and symptoms, several neurodegenerative \ndiseases-specifically, Alzheimer's (AD), Parkinson's (PD), and Huntington's \ndiseases (HDs)-share the common feature of abnormal circadian rhythms, such as \nthose in behavior (e.g., disrupted sleep/wake cycles), physiological processes \n(e.g., diminished hormone release) and biochemical activities (e.g., antioxidant \nproduction). Circadian disturbances are among the earliest symptoms of these \ndiseases, and the molecular mechanisms of the circadian system are suspected to \nplay a pivotal, and possibly causal, role in their natural histories. Here, we \nreview the common circadian abnormalities observed in ADs, PDs and HDs, and \nsummarize the evidence that the molecular circadian clockwork directly \ninfluences the course of these disease states. On the basis of this research, we \nexplore several circadian-oriented interventions proposed as treatments for \nthese neurological disorders.\n\nDOI: 10.3389/fnagi.2017.00170\nPMCID: PMC5447688\nPMID: 28611660",
  "journal": "Front Aging Neurosci",
  "year": 2017,
  "authors": "Hood S, Amir S",
  "url": "https://pubmed.ncbi.nlm.nih.gov/28611660/",
  "external_ids": {
    "doi": "10.3389/fnagi.2017.00170",
    "pmid": "28611660"
  },
  "citation_count": 0
}