Vascular dementia. Advances in nosology, diagnosis, treatment and prevention

Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD...

Full description

Saved in:
Bibliographic Details
Published inPanminerva medica Vol. 46; no. 4; p. 207
Main Author Román, G C
Format Journal Article
LanguageEnglish
Published Italy 01.12.2004
Subjects
Biomarkers
Cholinesterase Inhibitors - therapeutic use
Cognition Disorders - classification
Cognition Disorders - diagnosis
Cognition Disorders - prevention & control
Cognition Disorders - therapy
Dementia, Vascular - classification
Dementia, Vascular - diagnosis
Dementia, Vascular - prevention & control
Dementia, Vascular - therapy
Humans
Hypertension - prevention & control
Hypertension - therapy
Memantine - therapeutic use
Risk Factors
Stroke - prevention & control
Stroke - therapy
Online AccessGet more information

Cover

More Information
Summary:Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD). Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-tau was normal. CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD.
ISSN:0031-0808