The aim of this 12-month prospective study was to establish whether severe internal carotid artery stenosis is associated with faster progression of the cognitive impairment in patients with Alzheimer's disease (AD). Four hundred and eleven patients

Objectives: To evaluate cognitive performance in subjects with bilateral asymptomatic carotid stenosis (B-ACS) compared to subjects with unilateral ACS and to subjects with no carotid stenosis (CS) and to explore the relationship between cognitive performance and cerebral hemodynamics status in B-ACS. Methods: The neuropsychological investigation included phonemic (ph) and categorical (ca) Verbal Fluency (VF) tests for exploring the left brain functions and Colored Progressive Matrices (CPM) and Complex Figure Copy Test (CFCT) for the right brain. Cerebral hemodynamics status was assessed using the transcranial Doppler–based breath-holding index test. Results: A total of 333 subjects were included: 127 B-ACS, 73/77 left/right unilateral ACS, 56 no CS, mean age 70 ± 3.78 years, 65 male. Subjects with B-ACS and subjects with unilateral ACS showed significantly lower scores in all cognitive tests compared to subjects with no CS (p < 0.05). Subjects with B-ACS with left impaired hemodynamics status showed a significantly reduced ph-VF score, from 13.4 (95% confidence interval [CI] 11.2–15.8) to 7.5 (95% CI 5.4–9.7), and a reduced ca-VF score, from 19.7 (95% CI 18.1–24.1) to 10.8 (95% CI 9.5–15.1), compared to subjects with no CS. Similarly, impaired cerebral hemodynamics in the right side was associated with a significantly reduced CPM score, from an estimated mean of 34.2 (95% CI 29.8–35.4) to 24.6 (95% CI 20.2–25.8), and CFCT score from 37.0 (95% CI 32.0–37.4) to 27.1 (95% CI 23.3–28.7). All comparisons were p < 0.05. Conclusion: Subjects with B-ACS and subjects with unilateral ACS are more likely to have cognitive dysfunction compared to subjects with no CS. There appears to be a link between cognitive dysfunction and hemodynamics impairment due to carotid stenosis.

There is strong evidence that homocysteine is a risk factor not only for cerebrovascular diseases but also for degenerative dementias. A recent consensus statement renewed the importance and the role of high levels of homocysteine in cognitive decline in several forms of degenerative dementia, such as Alzheimer’s disease. Although the molecular mechanisms by which homocysteine causes cell dysfunction are known, both the impact of homocysteine on specific cognitive functions and the relationship between homocysteine level and non-Alzheimer dementias have been poorly investigated. Most of the studies addressing the impact of hyperhomocysteinemia on dementias have not examined the profile of performance across different cognitive domains, and have only relied on screening tests, which provide a very general and coarse-grained picture of the cognitive status of the patients. Yet, trying to understand whether hyperhomocysteinemia is associated with the impairment of specific cognitive functions would be crucial, as it would be, in parallel, learning whether some brain circuits are particularly susceptible to the damage caused by hyperhomocysteinemia. These steps would allow one to (i) understand the actual role of homocysteine in the pathogenesis of cognitive decline and (ii) improve the diagnostic accuracy, differential diagnosis and prognostic implications. This review is aimed at exploring and revising the state of the art of these two strictly related domains. Suggestions for future research are provided.

Epidemiological studies have suggested a pathophysiological link between obstructive sleep apnea syndrome (OSAS) and Alzheimer's disease (AD). The mechanism by which sleep disturbance can affect cognitive impairment is not clear. The aim of this stud