Publications by authors named "Rulin Geng"

With the development of society, the incidence of dementia and type 2 diabetes (T2DM) in the elderly has been increasing. Although the correlation between T2DM and mild cognitive impairment (MCI) has been confirmed in the previous literature, the interaction mechanism remains to be clarified. To explore the co-pathogenic genes in the blood of MCI and T2DM patients, clarify the correlation between T2DM and MCI, achieve the purpose of early disease prediction, and provide new ideas for the prevention and treatment of dementia.

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Background: Alzheimer's disease (AD), type 2 diabetes mellitus (T2DM), and Major Depressive Disorder (MDD) have a higher incidence rate in modern society. Although increasing evidence supports close associations between the three, the mechanisms underlying their interrelationships remain elucidated.

Objective: The primary purpose is to explore the shared pathogenesis and the potential peripheral blood biomarkers for AD, MDD, and T2DM.

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Diabetes mellitus (DM) is known to be a risk factor for dementia, especially in the elderly population, and close associations between diabetes and Alzheimer disease (AD) have been determined. Peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonists are insulin-sensitising drugs. In addition to their anti-diabetic properties, their effectiveness in preventing and decreasing cognitive impairment are the most recent characteristics that have been studied.

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Background: The many studies revealing a connection between serum uric acid (SUA) and dementia have reported conflicting results. This study sought to investigate the relations between SUA and cognitive function in older adults.

Materials And Methods: The sample was 2,767 American adults aged ≥60 years from the National Health and Nutrition Examination Survey 2011-2014.

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Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disease characterized by memory loss, inability to carry out everyday daily life, and noticeable behavioral changes. The essential neuropathologic criteria for an AD diagnosis are extracellular β-amyloid deposition and intracellular accumulation of hyperphosphorylated tau. However, the exact pathogenic mechanisms underlying AD remain elusive, and current treatment options show only limited success.

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