Vascular Cognitive Disorder. A Biological and Clinical Overview
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Although vascular dementia (VaD) represents the second most common cause of dementia after Alzheimer’s disease (AD) in the elderly, and is referred as the “silent epidemic of the twenty-first century”, there is still a controversy on terminology, classification and diagnostic criteria of VaD. The diagnosis of VaD resides in clinical criteria determining a cognitive impairment, the presence of cerebrovascular disease and, only in the case of post-stroke dementia or multi-infarct dementia, a temporal relationship between these. The search for a reliable biochemical tests helping in the diagnosis of VaD is so far not available. Several vascular risk factors have a role in the development of VaD and their identification and treatment are among the major aspects of management of VaD. A new line of research in this field is the study of genetic factors underlying vascular cognitive impairment which are: (1) genes predisposing to cerebrovascular disease, and (2) genes that influence brain tissue responses to cerebrovascular lesions. Evidence in favour of a coexistence of vascular and degenerative components in the pathogenesis of dementia in an elderly population comes from neuropathological and epidemiological studies. There is now a great debate whether VaD and AD are more than common coexisting unrelated pathologies and, instead, represent different results of synergistic pathological mechanisms. Preventive approaches aiming at reducing incident VaD by targeting patients at risk of cerebrovascular disease (primary prevention), or acting on patients after a stroke (secondary prevention) to prevent stroke recurrence and the progression of brain changes associated with cognitive impairment are mandatory therapeutic strategies.
KeywordsVascular cognitive disorder Biomarkers Alzheimer’s disease Risk factors
This work was supported in part by a grant from the Italian Ministry of Health within the Finalized Research Projects 2006–2007 (type II, No. 107). This paper is intended to honor Dr. Abel Lajtha, who founded this journal many years ago and directed it in a superb way from the beginning. Abel Lajtha did a lot of outstanding research in many fields, and particularly on protein metabolism and on transport of metabolites through nerve cells membranes, and his contributions have been of absolute relevance for the progress of our knowledge in both basic and clinical neurosciences. He has been President of the American and of the International Society for Neurochemistry as well as of many other International Societies in neurosciences. He also received many awards and I like to remember especially the one given by the University of Padova, that is the laurea “honoris causa” in Medicine. I also like to recall his continuous and quite established relationship with the scientific community of neuroscientists in Italy; many of us worked and trained in the neuroscience in his lab and under his precious guidance. In this acknowledgement, certainly incomplete, I would like to add a few personal words, that is a really deep and warm thanks to him for what he has taught me and given to me; he has taught me both science and humanity, that is well being, and he has given to me his affection and his friendship, extended also to my family. I’m really very grateful forever, and I like to say a warm thank to Abel Lajtha.
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