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Abstract
VaD is the loss of cognitive functions to a degree that interferes with ADLs, resulting from ischemic or hemorrhagic CVD or from cardiovascular or circulatory disturbances that injure brain regions that are important for memory, cognition and behavior. Although the increasing interest in the fields of public health as well as in research, there is still a great confusion on terminology, classification and diagnostic criteria of VaD (Roman, 2002). It is responsible for about 20% of cases of dementia in the elderly, second only to AD; also, vascular lesions are commonly found in the very old with AD pathology (Zekry et al., 2003).
from a public health viewpoint, recognition of VCI before the development of dementia and correction of vascular burden on the brain may lead to a global decrease of incident dementia (Erkinjuntti et al., 2004). But the major obstacle to the diagnosis of VaD is the complex nosological concept encompasses many clinical syndromes that result from a variety of pathogenic mechanisms that lead to different cognitive syndromes with varying evolution and progression. As as a result, no consensus has been reached on the pathological diagnosis of VaD (Korczyn, 2002).
The clinical syndromes of VaD may be divided simply into two main groups, acute and subacute, according to the temporal profile of clinical presentation. Acute-onset VaD includes patients with new-onset dementia after a clinically eloquent acute cerebrovascular event. The causal stroke is either a single strategic stroke resulting from occlusion (or rupture) of a large-size vessel or a symptomatic subcortical lacunar stroke caused by occlusive small-vessel disease. The older term MID is sometimes used when VaD develops after recurrent large-vessel strokes (Roman, 2005).
In VaD there is no single, classical cognitive and neurobehavioral phenotype since vascular brain injury may affect any region of the brain. In practice, it is widely accepted that at least in VaD, due to cerebral small vessels disease and hypoperfusion, patients present with a peculiar cognitive syndrome distinct from that seen in AD and characterized by predominant executive deficits (Looi and Sachdev, 1999).
An integrative approach to VaD diagnosis based on all the available evidence (history, vascular risk factors, physical exam, clinical course, neuroimaging, cognitive impairment pattern) is recommended (Robillard, 2007).
The use of a cut-off value for global cognitive scales is a frequent alternative approach to the diagnosis of dementia, particularly in large-scale studies (Madureira et al., 2006).
The search for biomarkers of late-life mental disorders includes the exploration of structural neuroimaging, functional neuroimaging, genomics, noninvasive neuro-physiology, CSF and plasma analysis. Biomarker research in late-life mental disorders is progressing at a rapid pace. The application of current biomarkers to clinical practice may be on the horizon with further research that refines their sensitivity and specificity (Daniel et al., 2008).
Combining structural imaging and functional imaging techniques may be helpful in differentiating VaD from AD. The minimum goal of MRI is to demonstrate infarcts and WML. Additional information, which can be useful in determining the age of infarcts, comes from DWI and MR angiography. PET can be used to differentiate VaD from AD (Semplicini et al., 2005).
Hyperhomocysteinemia and low levels of folic acid were significantly more frequent in both subcortical VaD and MID patients (Graban et al., 2009).
Carnosinase could differentiate “pure” AD from VaD, which cannot be achieved with either CSF amyloid-β1-42 or CSF total tau (Balion et al., 2007).
There has been evidence that the CSF level of MMP-9 is significantly increased in VaD patients compared to those with AD or to healthy elderly subjects (Adair et al., 2004).
The (amyloid-β42/ tau protein ratio) is an applicable method with cutoff values to identify individuals at increased risk of conversion to MCI which may be useful to people weighing the risk-benefit ratio of new preventive therapeutics (Li et al., 2007).
Genetic influences in VaD are primarily polygenic, although several monogenic disorders causing stroke have been identified. The clearest example of a monogenic disorder causing small artery stroke and VaD is CADASIL (Kalimo et al., 2002).