Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment

Gabor A. Fulop, Stefano Tarantini, Andriy Yabluchanskiy, Andrea Molnar, Calin I. Prodan, Tamas Kiss, Tamas Csipo, Agnes Lipecz, Priya Balasubramanian, E. Farkas, Peter Toth, Farzaneh Sorond, Anna Csiszar, Zoltan Ungvari

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

There has been an increasing appreciation of the role of vascular contributions to cognitive impairment and dementia (VCID) associated with old age. Strong preclinical and translational evidence links age-related dysfunction and structural alterations of the cerebral arteries, arterioles, and capillaries to the pathogenesis of many types of dementia in the elderly, including Alzheimer’s disease. The low-pressure, low-velocity, and large-volume venous circulation of the brain also plays critical roles in the maintenance of homeostasis in the central nervous system. Despite its physiological importance, the role of age-related alterations of the brain venous circulation in the pathogenesis of vascular cognitive impairment and dementia is much less understood. This overview discusses the role of cerebral veins in the pathogenesis of VCID. Pathophysiological consequences of age-related dysregulation of the cerebral venous circulation are explored, including blood-brain barrier disruption, neuroinflammation, exacerbation of neurodegeneration, development of cerebral microhemorrhages of venous origin, altered production of cerebrospinal fluid, impaired function of the glymphatics system, dysregulation of cerebral blood flow, and ischemic neuronal dysfunction and damage. Understanding the age-related functional and phenotypic alterations of the cerebral venous circulation is critical for developing new preventive, diagnostic, and therapeutic approaches to preserve brain health in older individuals.

Original languageEnglish
Pages (from-to)H1124-H1140
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume316
Issue number5
DOIs
Publication statusPublished - May 1 2019

Fingerprint

Cerebrovascular Circulation
Blood Vessels
Dementia
Brain
Cerebral Veins
Cerebral Arteries
Arterioles
Blood-Brain Barrier
Cerebrospinal Fluid
Alzheimer Disease
Homeostasis
Central Nervous System
Maintenance
Pressure
Cognitive Dysfunction
Health

Keywords

  • Cerebral circulation
  • Senescence
  • Vascular cognitive impairment
  • Vascular contributions to cognitive impairment and dementia
  • Vein

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment. / Fulop, Gabor A.; Tarantini, Stefano; Yabluchanskiy, Andriy; Molnar, Andrea; Prodan, Calin I.; Kiss, Tamas; Csipo, Tamas; Lipecz, Agnes; Balasubramanian, Priya; Farkas, E.; Toth, Peter; Sorond, Farzaneh; Csiszar, Anna; Ungvari, Zoltan.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 316, No. 5, 01.05.2019, p. H1124-H1140.

Research output: Contribution to journalArticle

Fulop, GA, Tarantini, S, Yabluchanskiy, A, Molnar, A, Prodan, CI, Kiss, T, Csipo, T, Lipecz, A, Balasubramanian, P, Farkas, E, Toth, P, Sorond, F, Csiszar, A & Ungvari, Z 2019, 'Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment', American Journal of Physiology - Heart and Circulatory Physiology, vol. 316, no. 5, pp. H1124-H1140. https://doi.org/10.1152/ajpheart.00776.2018
Fulop, Gabor A. ; Tarantini, Stefano ; Yabluchanskiy, Andriy ; Molnar, Andrea ; Prodan, Calin I. ; Kiss, Tamas ; Csipo, Tamas ; Lipecz, Agnes ; Balasubramanian, Priya ; Farkas, E. ; Toth, Peter ; Sorond, Farzaneh ; Csiszar, Anna ; Ungvari, Zoltan. / Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment. In: American Journal of Physiology - Heart and Circulatory Physiology. 2019 ; Vol. 316, No. 5. pp. H1124-H1140.
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