Journalartikel

Jahr der Veröffentlichung: 2016

Seiten: 1588-1603

Zeitschrift: Journal of Neuroscience Research

Bandnummer: 94

Heftnummer: 12

ISSN: 0360-4012

DOI Link: https://doi.org/10.1002/jnr.23925

Verlag: Wiley

Abstract: 
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.

Harvard-Zitierstil: Calabrese, V., Giordano, J., Signorile, A., Ontario, M., Castorina, S., De Pasquale, C., et al. (2016) Major Pathogenic Mechanisms in Vascular Dementia: Roles of Cellular Stress Response and Hormesis in Neuroprotection, Journal of Neuroscience Research, 94(12), pp. 1588-1603. https://doi.org/10.1002/jnr.23925

APA-Zitierstil: Calabrese, V., Giordano, J., Signorile, A., Ontario, M., Castorina, S., De Pasquale, C., Eckert, G., & Calabrese, E. (2016). Major Pathogenic Mechanisms in Vascular Dementia: Roles of Cellular Stress Response and Hormesis in Neuroprotection. Journal of Neuroscience Research. 94(12), 1588-1603. https://doi.org/10.1002/jnr.23925