Current Alzheimer Research - Online First
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Therapeutic Advances in Alzheimer’s Disease: Integrating Natural, Semi-Synthetic, and Synthetic Drug Strategies
Authors: Brijesh Singh Chauhan, Yash Pal Singh, Burkhard Poeggeler and Sandeep Kumar SinghAvailable online: 29 May 2025More LessAlzheimer’s disease (AD) is a neurodegenerative disorder associated with age, marked by progressive memory loss linked to the decline of cholinergic neurons, accumulation of amyloid plaques, and the presence of Neurofibrillary Tangles (NFTs). Neuropil threads in the brain contribute to amyloidosis and dementia. Despite extensive research, AD’s etiology remains unclear, and currently, no promising therapy exists. This review examines the role of natural, semi-synthetic, and synthetic drugs in AD treatment. Natural drugs demonstrate safety and efficacy with minimal adverse effects, while most agents, whether natural or synthetic, target multiple steps or directly counteract amyloidogenesis, tau protein pathology, oxidative stress, NMDA receptor activity, inflammation, acetylcholine (AChE) function, or α, β, γ secretase activity. In pursuit of improved treatment outcomes, we explore the effectiveness and challenges of various therapeutic interventions. Our hypothesis underscores the importance of an integrated approach combining these drug types for tailored symptom relief, suggesting combined therapies may offer greater therapeutic benefits compared to single-drug approaches. The drugs discussed show potential in regulating AD, thereby presenting viable options for its management. However, to obtain more favorable results, additional studies are needed by combining these drugs.
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Anthocyanidins Intake is Associated with Alzheimer’s Disease Risk in Americans over 60 Years of Age: Data from NHANES 2007-2008, 2009-2010, and 2017-2018
Authors: Yan Chen, Jingyi Zhao, Chen Li, Yinhui Yao and Yazhen ShangAvailable online: 29 May 2025More LessObjectiveAt present, there is limited research on the association between dietary intake of anthocyanidins and Alzheimer's disease (AD). More epidemiological studies are needed to better understand this relationship.
MethodsWe explored the relationship between dietary Anthocyanidins intake and AD among 3806 American adults in the National Health and Nutrition Examination Survey (NHANES) and the United States Department of Agriculture’s Food and Nutrient Database for Dietary Studies (FNDDS) from 2007 to 2010, and 2017 to 2018. We use weighted logistic regression model, restricted cubic spline (RCS) and weighted quantile sum (WQS) regression analysis to analyze the relationship between anthocyanidins monomer and AD.
ResultsThe weighted logistic regression model showed that the total intake of anthocyanidins was the fourth (OR:0.979; 95% CI: 0.966-0.992) quantile (relative to the lowest quantile) is related to the reduction of AD risk. RCS analysis showed that the total intake of anthocyanidins was negatively linearly correlated with AD (nonlinear P value was 0.002). The WQS regression analysis shows that cyanidin and malvidin are the main contributors to the comprehensive effects of six anthocyanidins.
DiscussionOur findings indicate that higher dietary anthocyanin intake may reduce the risk of AD and alleviate neurodegenerative processes. However, the mechanisms underlying this relationship remain unclear. Future studies should confirm these associations and investigate the relevant biological pathways.
ConclusionOur results show that a higher dietary intake of anthocyanidins is associated with a lower risk of AD.
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Quantitative Proteomic Analysis of APP/PS1 Transgenic Mice
Authors: Jiayuan Wang, Xinyu Wang, Zihui An, Xuan Wang, Yaru Wang, Yuehan Lu, Mengsheng Qiu, Zheqi Liu and Zhou TanAvailable online: 02 December 2024More LessBackgroundAlzheimer's disease (AD) is a prevalent neurodegenerative disorder affecting the central nervous system (CNS), with its etiology still shrouded in uncertainty. The interplay of extracellular amyloid-β (Aβ) deposition, intracellular neurofibrillary tangles (NFTs) composed of tau protein, cholinergic neuronal impairment, and other pathogenic factors is implicated in the progression of AD.
ObjectiveThe current study endeavors to delineate the proteomic landscape alterations in the hippocampus of an AD murine model, utilizing proteomic analysis to identify key physiological and pathological shifts induced by the disease. This endeavor aims to shed light on the underlying pathogenic mechanisms, which could facilitate early diagnosis and pave the way for novel therapeutic interventions for AD.
MethodsTo dissect the proteomic perturbations induced by Aβ and Presenilin-1 (PS1) in the AD pathogenesis, we undertook a label-free quantitative (LFQ) proteomic analysis focusing on the hippocampal proteome of the APP/PS1 transgenic mouse model. Employing a multi-faceted approach that included differential protein functional enrichment, cluster analysis, and protein-protein interaction (PPI) network analysis, we conducted a comprehensive comparative proteomic study between APP/PS1 transgenic mice and their wild-type C57BL/6 counterparts.
ResultsMass spectrometry identified a total of 4817 proteins in the samples, with 2762 proteins being quantifiable. Comparative analysis revealed 396 proteins with differential expression between the APP/PS1 and control groups. Notably, 35 proteins exhibited consistent temporal regulation trends in the hippocampus, with concomitant alterations in biological pathways and PPI networks.
ConclusionsThis study presents a comparative proteomic profile of transgenic (APP/PS1) and wild-type mice, highlighting the proteomic divergences. Furthermore, it charts the trajectory of proteomic changes in the AD mouse model across the developmental stages from 2 to 12 months, providing insights into the physiological and pathological implications of the disease-associated genetic mutations.
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Cognitive Reserve in Aging
Authors: A. M. Tucker and Y. Stern
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