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Vascular Dementia

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Abstract

Dementia is one of the most frequent disorders in the elderly. Its prevalence doubles every 5 years after the age of 65 years [1]. Vascular dementia (VaD), the second leading cause of dementia after Alzheimer’s disease (AD), is an important cause of chronic disability [2]. Until the 1950s, most dementias were attributed to atherosclerosis of cervical and cerebral arteries, leading to the old concept of chronic cerebral hypoperfusion. During the 1970s, AD progressively took the foreground, and the term multi-infarct dementia was introduced to emphasize that infarcts are necessary to induce VaD. The pendulum is now swinging back to the role of vascular factors in dementia [1], because of possible recognition and effective treatment during life. The term vascular dementia is now used for dementia syndromes likely to be the consequence of ischémic, hemorrhagic, or hypoxic lesions of the brain [3]. However, evidence of stroke does not necessarily mean a causal relationship [4]: vascular lesions of the brain are frequent in patients with Alzheimer’s pathology [4] and probably contribute to their cognitive decline [5]. VaD is now considered to be the core manifestation of a broad spectrum of clinical syndromes. This chapter focuses on recent advances in the field of VaD.

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Leys, D., Parnetti, L., Pasquier, F. (2001). Vascular Dementia. In: Fisher, M., Bogousslavsky, J. (eds) Current Review of Cerebrovascular Disease. Current Medicine Group, London. https://doi.org/10.1007/978-1-4684-0001-4_15

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