Current Alzheimer research最新文献

Alzheimer's disease (AD) is the most common type of dementia, pathologically characterized by the accumulation of senile plaques and neurofibrillary tangles. Chronic kidney disease (CKD) is highly prevalent in the elderly population closely associated with the occurrence of dementia. Recent epidemiological and experimental studies suggest a potential association of CKD with AD. Both diseases share a panel of identical risk factors, such as type 2 diabetes and hypertension. However, the relationship between CKD and AD is unclear. Lower clearance of a panel of uremic toxin including cystatin- C, guanidine, and adiponectin due to CKD is implied to contribute to AD pathogenesis. In this review, we summarize the current evidence from epidemiological, experimental, and clinical studies on the potential contribution of uremic toxins to AD pathogenesis. We describe outstanding questions and propose an outlook on the link between uremic toxins and AD.

Background: Alzheimer's disease (AD) is the most common form of dementia in the elderly population and places heavy burdens on medical care and nursing. Recently, the psychiatric and behavioral symptoms of prodromal AD, especially mild behavioral impairment (MBI), have attracted much attention. In 2012, Alzheimer's Association International Conference, MBI was proposed as a syndrome with psychiatric and behavioral disturbance before the onset of typical clinical cognitive symptoms in dementia. Increasing lines of evidence have indicated the link between MBI and early AD pathologies including Aβ and tau.

Objective: This narrative review aims to summarize the advantages of MBI over other concept of psychiatric and behavioral symptoms associated with AD in the early prediction of AD dementia. We also discuss the possible common genetic basis and pathological mechanisms underlying the interactions between MBI and AD.

Methods: Papers cited here were retrieved from PubMed up to February 2022. We selected a total of 95 articles for summary and discussion.

Results: The occurrence of MBI is mainly due to the overlapped genetic and pathological risk factors with AD and is related to the brain's response to environmental stressors. MBI may be a warning sign for the early pathology of AD, and more attention should be paid on the number and duration of MBI symptoms.

Conclusion: MBI may be an early sign and predictor of Alzheimer's disease dementia. Early intervention for MBI may have a positive effect on alleviating long-term cognitive decline.

Background: Neuroimaging suggests that white matter microstructure is severely affected in Alzheimer's disease (AD) progression. However, whether alterations in white matter microstructure are confined to specific regions and whether they can be used as potential biomarkers to distinguish normal control (NC) from AD are unknown.

Methods: In this cross-sectional study, 33 cases of AD and 25 cases of NC were recruited for automatic fiber quantification (AFQ). A total of 20 fiber bundles were equally divided into 100 segments for quantitative assessment of fractional anisotropy (FA), mean diffusivity (MD), volume and curvature. In order to further evaluate the diagnostic value, the maximum redundancy minimum (mRMR) and LASSO algorithms were used to select features, calculate the Radscore of each subject, establish logistic regression models, and draw ROC curves, respectively, to assess the predictive power of four different models.

Results: There was a significant increase in the MD values in AD patients compared with healthy subjects. The differences were mainly located in the left cingulum hippocampus (HCC), left uncinate fasciculus (UF) and superior longitudinal fasciculus (SLF). The point-wise level of 20 fiber bundles was used as a classification feature, and the MD index exhibited the best performance to distinguish NC from AD.

Conclusion: These findings contribute to the understanding of the pathogenesis of AD and suggest that abnormal white matter based on DTI-based AFQ analysis is helpful to explore the pathogenesis of AD.