Articles

This study finds that impaired cellular immune dysfunction in AD patients was significantly correlated with abnormal MRS, and neuroimmune dysfunction may contribute to the pathogenesis of AD and alter the metabolism of neurotransmitters such as aspartic acid and MI in the brains of AD patients.

This study reveals that Dl-3-n-butylphthalide (NBP) improves learning deficits and reduces Aβ plaque deposition in Alzheimer's disease (AD) transgenic mice by enhancing microglial activation and phagocytosis of Aβ plaques. The therapeutic effects of NBP are linked to the AGE-RAGE signaling pathway, demonstrating its potential in alleviating cognitive impairment and neuroinflammation in AD.

This study identified key biochemical pathways and protein changes in the Alzheimer's disease (AD) human hippocampus, revealing increased expression of proteins VGF, GFAP, HSPB1, and APP, with UBC being most centrally involved, and highlighted the roles of four hub proteins (CD44, APP, ITGB2, APOE) linked to amyloid plaques and two (RPL24, RPS23) to neurofibrillary tangles, along with the impact of modified proteins on immune activation and synaptic disruption, uncovering potential therapeutic targets involving specific proteins, microRNAs, and transcription factors.

This article summarizes current biomarkers, available treatments, and future therapeutic approaches for Alzheimer's disease, discussing drug targets like Amyloid β, Tau Protein, and various other mechanisms. Additionally, it highlights the historical use of Estradiol, outcomes of trials with antioxidants and omega-3 fatty acids, and ongoing clinical trials, providing a comprehensive overview of the evolving landscape in AD research and treatment.