Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations

miR155, triplicated in Down syndrome, regulates the development of neural stem cells and GABAergic interneurons in Alzheimer's disease mouse and human iPSC models

Dysfunctional microRNAs and GABAergic interneurons are features of Alzheimer's disease (AD). The role of neuronal microRNA155 (miR155), elevated in both AD and Down syndrome (DS), remains unknown.

Unraveling Neurodegeneration: Common Molecular Mechanisms and Novel Therapeutic Concepts in Major Neurodegenerative Disorders

This review sought to integrate disease‐specific causative triggers with shared pathogenic pathways, focusing on neuroinflammatory signaling, oxidative imbalance, mitochondrial impairment, and disrupted protein homeostasis, in order to support multi‐target, disease‐modifying therapeutic strategies.

Parkinson's gene linked to early dysfunction in brain cells

Epigenetic Mechanisms Underlying Cognitive Dysfunction in Parkinson's Disease: Current Evidence and Future Prospects

The purpose of this review is to explore how epigenetic alterations affect gene expression and their potential role in cognitive dysfunction associated with PD.

Elucidating the neuropathological and molecular heterogeneity of amyloid beta and tau in Alzheimer's disease through machine learning and transcriptomic integration

Functional brain network alterations associated with Alzheimer's disease (AD) pathology, including amyloid beta (Aβ) and phosphorylated tau (p‐tau), are difficult to interpret due to overlapping aging‐associated and non‐amyloid biological processes.

Combined Vitamin D and Resveratrol Treatment Attenuates Motor Deficits and Neurodegeneration in a 6‐OHDA Mouse Model of Parkinson's Disease in Male Mice: A Focus on Sirt1 and Lingo‐1 Pathways in the Ventral Tegmental Area

Given the neuroprotective properties of Vitamin D3 and resveratrol, this study examined whether their combined administration could modulate Sirt1 and Lingo‐1 expression and attenuate neurodegeneration in a 6‐hydroxydopamine (6‐OHDA) model of PD.