Advanced carotid disease is known to be associated with symptomatic cerebrovascular diseases, such as stroke or transient ischemic attack (TIA), as well as with poststroke cognitive impairment. However, cognitive decline often occurs in patients with advanced carotid stenosis without clinically evident stroke or TIA, so it is also suspected to be an independent risk factor for dementia. Neurosonological methods enable simple and noninvasive assessment of carotid stenosis in patients at risk of advanced atherosclerosis. Cognitive status in patients diagnosed with advanced carotid stenosis is routinely not taken into consideration, although if cognitive impairment is present, such patients should probably be called symptomatic. In this paper, we discuss results of some most important studies that investigated cognitive status of patients with asymptomatic advanced carotid disease and possible mechanisms involved in the causal relationship between asymptomatic advanced carotid disease and cognitive decline. 1. Introduction While detrimental effects of stroke on cognitive functions have been well documented in the literature, the mechanisms linking advanced carotid disease and impaired cognitive status in patients without symptomatic cerebrovascular incidents are less clear. Advanced carotid disease is associated with the presence of multiple vascular risk factors, which most often include arterial hypertension, dyslipidemia, cigarette smoking, diabetes, and older age [1–3]. The same risk factors were shown to be associated not only with vascular dementia, but also with neurodegenerative dementia, importantly with Alzheimer’s disease [4]. The vascular hypothesis of Alzheimer’s disease provides substantial evidence that vascular risk factors play a critical role in the development of cognitive impairment and clinically evident dementia during aging [4]. Vascular dementia and Alzheimer’s disease in their pure forms are two ends of a pathologic continuum [5]. However, many studies during the last decade implicated the overlap of their pathologies. It was shown that a substantial proportion of brains who meet neuropathological criteria for Alzheimer’s disease also demonstrate lesions typical for vascular pathology, such as cerebral amyloid angiopathy, microvascular degeneration, and periventricular white matter lesions [6, 7]. Results of the seminal “Nun Study” that followed 102 elderly nuns until postmortem showed higher prevalence of clinically expressed dementia in those who met neuropathological criteria for Alzheimer’s disease and simultaneously had brain
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