Older people with a genetic risk of Alzheimer's disease did not experience the expected increase in cognitive decline and dementia risk if they consumed relatively large amounts of meat. This is shown in a new study from Karolinska Institutet published in JAMA Network Open. The results may contribute to the development of more individually tailored dietary advice.

New treatments for neurodegenerative diseases like Alzheimer’s, Parkinson’s, and motor neurone disease (MND) could be unlocked thanks to microscopic medicines developed by researchers at the University of Essex. Using artificial intelligence, an international team of scientists has created tiny antibody fragments that can be made directly inside human cells, where they bind to proteins linked to disease. These redesigned molecules will be made freely available to other scientists now the research has been published in Nature Communications. 

A team from the University of Barcelona has designed and validated in animal models an innovative compound with a pioneering mechanism of action for the treatment of Alzheimer’s disease. Unlike current drugs, which mainly remove beta-amyloid plaques that accumulate in the brain, this new experimental drug reprogrammes the neuronal epigenome by correcting alterations in gene expression that contribute to the progression of the disease. The results of this study, published in Molecular Therapy, open the door to an epigenetic-based therapeutic strategy to fight Alzheimer’s disease.

This review examines the gut–brain axis (GBA) as a critical bidirectional network linking gut microbiota to brain function and pathology. It details key pathways—neural, immune, endocrine, and metabolic—through which gut-derived signals influence conditions like depression, Alzheimer’s, and Parkinson’s disease. The article highlights novel microbiota-targeted therapies, including probiotics, fecal transplantation, and dietary strategies, underscoring their potential for pioneering personalized approaches in neuropsychiatry. These hold promises for innovative treatments. Personalized medicine is the way forward.

Longitudinal follow-up reveals that a significant proportion of these lesions may stabilize or even decrease once Alzheimer’s disease symptoms are present, challenging the concept of exclusively cumulative vascular damage.

Published in Alzheimer’s & Dementia, one of the leading international journals in dementia research, the study provides new data on the interaction between vascular alterations, neurodegeneration, and beta-amyloid and tau proteins in the brain.

The findings reinforce the need to analyze Alzheimer’s disease from a temporal perspective, as the evolution of these lesions cannot be explained solely by the progression of classical biomarkers.