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

• Published in: Panminerva medica Vol. 46; no. 4; p. 207
• Main Author: Román, G C
• Format: Journal Article
• Language: English
• 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
• ISSN: 0031-0808

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.