Publications by authors named "A L Salami"

The cognitive neuroscience of human aging seeks to identify neural mechanisms behind the commonalities and individual differences in age-related behavioral changes. This goal has been pursued predominantly through structural or "task-free" resting-state functional neuroimaging. The former has elucidated the material foundations of behavioral decline, and the latter has provided key insight into how functional brain networks change with age.

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Although age differences in the dopamine system have been suggested to contribute to age-related cognitive decline based on cross-sectional data, recent large-scale cross-sectional studies reported only weak evidence for a correlation among aging, dopamine receptor availability, and cognition. Regardless, longitudinal data remain essential to make robust statements about dopamine losses as a basis for cognitive aging. We present correlations between changes in D2/3 dopamine receptor availability and changes in working memory measured over 5 yr in healthy, older adults (n = 128, ages 64 to 68 yr at baseline).

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Manganese (Mn), a trace element, has been documented to exert an important role in the metabolism of cholesterol. Cholesterol gallstone (CG) pathogenesis is directly linked to biliary cholesterol imbalance which could be due to diabetes complications or mismanagement. NF-κβ pathway, an inflammatory regulator, has been implicated in metabolic disease especially in the context of diabetes and gallstone formation.

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Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by progressive cognitive decline. Genetic factors have been implicated in disease susceptibility as its etiology remains multifactorial. The and the genes, involved in immune responses, have emerged as potential candidates influencing AD risk.

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Anti-Jo1 antibodies are usually known markers of myositis. However, they can be associated with different pathologies. We aimed to determine the immuno-clinical characteristics of patients with positive anti-Jo1.

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