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J Neurosci Res. 2016 Dec;94(12):1588-1603. doi: 10.1002/jnr.23925. Epub 2016 Sep 23.

Major pathogenic mechanisms in vascular dementia: Roles of cellular stress response and hormesis in neuroprotection.

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Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, Catania, Italy.
Departments of Neurology and Biochemistry and Neuroethics Studies Program, Pellegrino Center for Clinical Bioethics, Georgetown University Medical Center, Washington, DC.
Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari, Bari, Italy.
Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, Catania, Italy.
Department of Medical, Surgical Sciences and Advanced Technologies, University of Catania, Italy.
Institute of Nutrition Sciences, Justus-Liebig-University of Giessen, Giessen, Germany.
Department of Environmental Health Sciences, University of Massachusetts, Amherst, Amherst, Massachusetts.


Vascular dementia (VaD), considered the second most common cause of cognitive impairment after Alzheimer disease in the elderly, involves the impairment of memory and cognitive function as a consequence of cerebrovascular disease. Chronic cerebral hypoperfusion is a common pathophysiological condition frequently occurring in VaD. It is generally associated with neurovascular degeneration, in which neuronal damage and blood-brain barrier alterations coexist and evoke beta-amyloid-induced oxidative and nitrosative stress, mitochondrial dysfunction, and inflammasome- promoted neuroinflammation, which contribute to and exacerbate the course of disease. Vascular cognitive impairment comprises a heterogeneous group of cognitive disorders of various severity and types that share a presumed vascular etiology. The present study reviews major pathogenic factors involved in VaD, highlighting the relevance of cerebrocellular stress and hormetic responses to neurovascular insult, and addresses these mechanisms as potentially viable and valuable as foci of novel neuroprotective methods to mitigate or prevent VaD.


cell stress response; hormesis; inflammasome; neuroinflammation; neurovasculature; oxidative stress; vascular dementia; vitagenes

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