This article systematically summarizes the neuroprotective effects and mechanisms of ginsenosides Rg1, Rb1, and rare ginsenosides against Parkinson's disease (PD) and Alzheimer's disease (AD). The key findings indicate that ginsenosides exert their beneficial effects by modulating various signaling pathways related to inflammation, oxidative stress, apoptosis, and autophagy.

This review highlights how nurse practitioners can strengthen Alzheimer’s disease care by supporting earlier diagnosis and access to treatment, which is essential for maintaining quality of life. Expanding their role helps reduce barriers in the healthcare system, ensuring people with Alzheimer’s receive timely care that promotes better health and well-being.

The article presents PI4AD, a computational medicine framework that integrates multi-omics data, systems biology, and artificial neural networks to prioritize therapeutic targets for Alzheimer's disease (AD). PI4AD recovers clinically validated targets like APP and ESR1, confirming its prioritization efficacy. The framework identifies Ras signaling as a central therapeutic hub, complementing traditional amyloid/tau-focused approaches. Crosstalk analysis reveals critical nodal genes (e.g., HRAS and MAPK1) and drug repurposing opportunities, bridging genetic insights with pathway-level biology.

The article suggest that beta-amyloid protein (Aβ) has a significant indirect effect on neurogranin (Ng) through key synaptic mediators such as SYT1 and GAP43 during the preclinical stages of Alzheimer’s disease (AD). These findings highlight the crucial role of SYT1 and GAP43 in mediating beta-amyloid-induced synaptic dysfunction, offering potential early biomarkers and therapeutic targets for AD progression.

The article discusses the potential of artificial intelligence (AI) in revolutionizing drug discovery for Alzheimer's disease (AD) and delirium. It explores how AI can facilitate target identification, small molecule and protein-based drug design, and optimization of pharmacokinetic properties to address the challenges in developing effective treatments for these two brain diseases.

The article provides a comprehensive overview of the Keystone Symposia conference on Myeloid Cell Diversity, highlighting key presentations on topics such as phagocytosis of dead cells, neutrophil behavior, myeloid cell states, and the impact of lifestyle factors on myeloid cells in disease states. It also discusses the role of myeloid cells in Alzheimer's disease, specifically how their dissociation may mediate vascular dysfunction.

The article describes the development of a self-regulated multi-functional nano-modulator (siR/PIO@RP) that can intelligently navigate to the damaged blood-brain barrier and release therapeutic cargoes for synergetic Alzheimer's disease (AD) therapy. The nano-modulator is capable of reducing cerebral amyloid-β load, relieving neuroinflammation, and alleviating the dysfunction of the neurovascular unit, providing proof of concept that normalizing the neurovascular unit holds promise as a means of alleviating AD symptoms.

The article discusses the connection between type 2 diabetes mellitus (T2DM) and neurodegenerative disorders, with a focus on the role of mitochondrial dysfunction as a potential link between these conditions. It reviews the epidemiological and molecular evidence that suggests T2DM as a risk factor for the development of Alzheimer's disease and Parkinson's disease, and highlights the importance of understanding the mitochondrial mechanisms underlying this relationship to identify new therapeutic targets.

This cross-sectional population-based study examined the relationship between statin use and anti-Alzheimer's disease (AD) drug prescription in patients over 70 years old with cardiovascular risk factors. The key findings were: 1) Patients using low-potency or hydrophilic statins had lower odds of anti-AD medication usage compared to high-potency or lipophilic statins, respectively; 2) Patients taking rosuvastatin or pitavastatin had lower odds of anti-AD medication usage than those consuming atorvastatin.

In this review, Hu et al. summarize fluid biomarker findings across 12 anti-amyloid-β clinical trials. The emerging biomarker data provide evidence of impact of the new therapies on the underlying pathophysiological processes of the AD, supporting the presence of a disease-modifying effect.