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Inhaled xenon modulates microglia and ameliorates disease in mouse models of amyloidosis and tauopathy.
Sci Transl Med
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Antiamyloid antibody treatments modestly slow disease progression in mild dementia due to AD. Emerging evidence shows that homeostatic dysregulation of the brain immune system, especially that orchestrated by microglia, plays an important role in disease onset and progression.
View Article and Find Full Text PDFMotor involvement in frontotemporal lobar degeneration with TAR DNA-binding protein of 43 kDa type C.
Neuropathology
January 2025
Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan.
The degeneration of pyramidal tracts has been reported in frontotemporal lobar degeneration with TDP-43 (TAR DNA-binding protein 43) pathology (FTLD-TDP) type C. Herein, we examined the detailed pathology of the primary motor area and pyramidal tracts in the central nervous system in four autopsy cases of FTLD-TDP type C, all of which were diagnosed by neuropathological, biochemical, and genomic analyses. Three patients showed right dominant atrophy of the frontal and temporal lobes, while the other patient showed left dominant atrophy.
View Article and Find Full Text PDFThe MR1/MAIT cell axis enhances dystrophic neurite development in Alzheimer's disease.
Alzheimers Dement
January 2025
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Introduction: Plaques are a hallmark feature of Alzheimer's disease (AD). We found that the loss of mucosal-associated invariant T (MAIT) cells and their antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting dystrophic neurites.
View Article and Find Full Text PDFPreferential clustering of microglia and astrocytes around neuritic plaques during progression of Alzheimer's disease neuropathological changes.
J Neurochem
January 2025
Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, Florida, USA.
Neuroinflammation plays an important role in the pathological cascade of Alzheimer's disease (AD) along with aggregation of extracellular amyloid-β (Aβ) plaques and intracellular aggregates of tau protein. In animal models of amyloidosis, local immune activation is centered around Aβ plaques, which are usually of uniform morphology, dependent on the transgenic model used. In postmortem human brains a diversity of Aβ plaque morphologies is seen including diffuse plaques (non-neuritic plaques, non-NP), dense-core plaques, cotton-wool plaques, and NP.
View Article and Find Full Text PDFIntegrative pathway analysis across humans and 3D cellular models identifies the p38 MAPK-MK2 axis as a therapeutic target for Alzheimer's disease.
Neuron
November 2024
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA; McCance Center for Brain Health, Massachusetts General Hospital, Boston, MA 02114, USA. Electronic address:
Article Synopsis
- Alzheimer's disease (AD) poses significant treatment challenges, particularly targeting amyloid-β (Aβ), but a new analysis method uncovered 83 dysfunctional pathways relevant to AD in both human brains and lab models.
- The p38 MAPK pathway was notably upregulated and linked to tau pathology and neuronal damage, highlighting its potential as a therapeutic target.
- By using integrative pathway activity analysis (IPAA), researchers can combine human data with cellular models to efficiently identify promising drug targets for AD treatment.*
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