Vascular cognitive impairment, dementia, aging and energy demand. A vicious cycle

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• 作者：A. Popa-Wagner ; Ana-Maria Buga ; B. Popescu ; D. Muresanu
• 关键词：Vascular cognitive impairment ; Vascular dementia ; Alzheimer’s disease ; Neurovascular unit ; Glucose consumption ; Insulin signaling
• 刊名：Journal of Neural Transmission
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：122
• 期：1-supp
• 页码：47-54
• 全文大小：2,824 KB
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• 作者单位：A. Popa-Wagner (1) (6)
  Ana-Maria Buga (1)
  B. Popescu (2) (3) (4)
  D. Muresanu (5)
  
  1. Department of Psychiatry, University of Medicine, Rostock, Germany
  6. Department of Functional Sciences, University of Medicine and Pharmacy, Petru Rares No 2, 200349, Craiova, Romania
  2. Department of Neurology, Neurosurgery and Psychiatry, ‘Carol Davila’ University of Medicine and Pharmacy, Bucharest, Romania
  3. Clinical Department of Neurology, Colentina Clinical Hospital, CDPC, Bucharest, Romania
  4. Laboratory of Molecular Medicine and Neuroscience, ‘Victor Babeș’ National Institute of Pathology, Bucharest, Romania
  5. Department of Neurology, University of Medicine and Pharmacy, Cluj-Napoca, Romania
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Neurology
  Pharmacology and Toxicology
  Psychiatry
  
• 出版者：Springer Wien
• ISSN：1435-1463

文摘

To a great extent, cognitive health depends on cerebrovascular health and a deeper understanding of the subtle interactions between cerebrovascular function and cognition is needed to protect humans from one of the most devastating affliction, dementia. However, the underlying biological mechanisms are still not completely clear. Many studies demonstrated that the neurovascular unit is compromised in cerebrovascular diseases and also in other types of dementia. The hemodynamic neurovascular coupling ensures a strong increase of the cerebral blood flow (CBF) and an acute increase in neuronal glucose uptake upon increased neural activity. Dysfunction of cerebral autoregulation with increasing age along with age-related structural and functional alterations in cerebral blood vessels including accumulation of amyloid-beta (Aβ) in the media of cortical arterioles, neurovascular uncoupling due to astrocyte endfeet retraction, impairs the CBF and increases the neuronal degeneration and susceptibility to hypoxia and ischemia. A decreased cerebral glucose metabolism is an early event in Alzheimer’s disease (AD) pathology and may precede the neuropathological Aβ deposition associated with AD. Aβ accumulation in turn leads to further decreases in the CBF closing the vicious cycle. Alzheimer, aging and diabetes are also influenced by insulin/insulin-like growth factor-1 signaling, and accumulated evidence indicates sporadic AD is associated with disturbed brain insulin metabolism. Understanding how vascular and metabolic factors interfere with progressive loss of functional neuronal networks becomes essential to develop efficient drugs to prevent cognitive decline in elderly.