A rare variant of Apolipoprotein E3 with neuroprotective properties has been identified in autosomal-dominant Alzheimer's disease. In this issue of Neuron, Chen et al. show that direct interaction between this variant and tau blocks tau pathogenesis in rodent models.
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Unraveling the mystery of citrate transporters in Alzheimer's disease: An updated review.
Ageing Res Rev
March 2025
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430. Electronic address:
A key molecule in cellular metabolism, citrate is essential for lipid biosynthesis, energy production, and epigenetic control. The etiology of Alzheimer's disease (AD), a progressive neurodegenerative illness marked by memory loss and cognitive decline, may be linked to dysregulated citrate transport, according to recent research. Citrate transporters, which help citrate flow both inside and outside of cells, are becoming more and more recognized as possible participants in the molecular processes underlying AD.
View Article and Find Full Text PDFThe role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer's disease.
Front Aging Neurosci
February 2025
Hospital of Encephalopathy, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Alzheimer's disease (AD) is a severe neurodegenerative disease characterized mainly by the formation of amyloid beta (Aβ) plaques and abnormal phosphorylation of tau. In recent years, an imbalance in iron homeostasis has been recognized to play a key role in the pathological process of AD. Abnormal iron accumulation can activate various kinases such as glycogen synthase kinase-3β, cyclin-dependent kinase 5, and mitogen-activated protein kinase, leading to abnormal phosphorylation of tau and amyloid precursor protein, and accelerating the formation of Aβ plaques and neurofibrillary tangles.
View Article and Find Full Text PDFDepletion of nuclear cytoophidia in Alzheimer's disease.
Free Neuropathol
January 2025
Department of Laboratory Medicine, St. Michael's Hospital, Unity Health & Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
There is considerable evidence for a role for metabolic dysregulation, including disordered purine nucleotide metabolism, in the pathogenesis of Alzheimer's disease (AD). Purine nucleotide synthesis in the brain is regulated with high fidelity to co-ordinate supply with demand. The assembly of some purine biosynthetic enzymes into linear filamentous aggregates called "cytoophidia" (Gk.
View Article and Find Full Text PDFExamining the effects of extremely low-frequency magnetic fields on cognitive functions and functional brain markers in aged mice.
Sci Rep
March 2025
Institut de Neurosciences Cognitives et Intégratives d'Aquitaine, CNRS UMR 5287, Université de Bordeaux and Ecole Pratique des Hautes Etudes, 33000, Bordeaux, France.
Extremely low-frequency magnetic fields (ELF-MFs) are ubiquitously present in various environments of everyday life. While surveys from the World Health Organization (WHO) have not demonstrated the existence of ELF-MF-induced harmful consequences in healthy subjects, whether older adults are more vulnerable to the effects of residential and occupational ELF-MF exposure, and therefore may be at risk, remains unsettled. Here, we explored this potential health issue by investigating, in aged mice, the effects of chronic exposure to ELF-MFs (50 Hz ELF-MF at 1 mT for 8 h/day, 5 days/week for 12 consecutive weeks) on cognitive functions and expression profile of brain markers typically associated with aggravated aging or the development of Alzheimer`s disease (AD).
View Article and Find Full Text PDFPorphyromonas gingivalis outer membrane vesicles alter cortical neurons and Tau phosphorylation in the embryonic mouse brain.
PLoS One
March 2025
Institute for Genomic Medicine, Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Porphyromonas gingivalis (Pg) is an oral bacterial pathogen that has been associated with systemic inflammation and adverse pregnancy outcomes such as low birth weight and pre-term birth. Pg drives these sequelae through virulence factors decorating the outer membrane that are present on non-replicative outer membrane vesicles (OMV) that are suspected to be transmitted systemically. Given that Pg abundance can increase during pregnancy, it is not well known whether Pg-OMV can have deleterious effects on the brain of the developing fetus.
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