T2 relaxation time (T2) alterations may serve as markers for early detection and disease progression monitoring by reflecting brain microstructural integrity in Alzheimer's disease (AD). However, the characteristics of T2 alterations during the early stage of AD remain elusive. We explored T2 alterations and their possible correlations with cognitive function in 5XFAD mice at early ages (1, 2, 3, and 5 months of age). Voxel-based analysis (VBA) and region of interest (ROI) analysis showed a decreased T2 in the hippocampus of 2-, 3-, and 5-month-old 5XFAD mice compared to those of controls. The dorsal hippocampal T2 decreased earlier than the ventral hippocampus T2. A significant correlation was observed between Morris water maze (MWM) test cognitive behavior and the dorsal hippocampus T2 in 5XFAD mice. These results indicated that the microstructural integrity of brain tissues, particularly the hippocampus, was impaired early and the impairment became more extensive and severe during disease progression. Furthermore, the dorsal hippocampus is a crucial component involved in spatial cognition impairment in young 5XFAD mice.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.brainresbull.2019.08.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.
Mol Neurodegener
January 2025
Department of Neurobiology and Behavior, Charlie Dunlop School of Biological Sciences, University of California, Irvine, CA, 92697-4545, USA.
Background: Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer's Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects.
View Article and Find Full Text PDFParental origin of transgene modulates amyloid-β plaque burden in the 5xFAD mouse model of Alzheimer's disease.
Neuron
January 2025
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Electronic address:
In Alzheimer's disease (AD) research, the 5xFAD mouse model is commonly used as a heterozygote crossed with other genetic models to study AD pathology. We investigated whether the parental origin of the 5xFAD transgene affects plaque deposition. Using quantitative light-sheet microscopy, we found that paternal inheritance of the transgene led to a 2-fold higher plaque burden compared with maternal inheritance, a finding consistent across multiple 5xFAD colonies.
View Article and Find Full Text PDFApoE3 R136S binds to Tau and blocks its propagation, suppressing neurodegeneration in mice with Alzheimer's disease.
Neuron
January 2025
Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; Faculty of Life and Health Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, Guangdong, China; Faculty of Life and Health Sciences, Shenzhen University of Advanced Technology (SUAT), Shenzhen 518055, Guangdong, China. Electronic address:
PSEN1 E280A carrier for the APOE3 Christchurch variant (R136S) is protected against Alzheimer's disease (AD) symptoms with a distinct anatomical pattern of Tau pathology. However, the molecular mechanism accounting for this protective effect remains incompletely understood. Here, we show that the ApoE3 R136S mutant strongly binds to Tau and reduces its uptake into neurons and microglia compared with ApoE3 wild type (WT), diminishing Tau fragmentation by asparagine endopeptidase (AEP), proinflammatory cytokines by Tau pre-formed fibrils (PFFs) or β-amyloid (Aβ), and neurotoxicity.
View Article and Find Full Text PDFInhaled 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 PDFNR1D1 Inhibition Enhances Autophagy and Mitophagy in Alzheimer's Disease Models.
Aging Dis
January 2025
Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway.
Alzheimer's disease (AD) is marked by extracellular beta-amyloid (Aβ) plaques and intracellular Tau tangles, leading to progressive cognitive decline and neuronal dysfunction. Impaired autophagy, a process by which a cell breaks down and destroys damaged or abnormal proteins and other substances, contributes to AD progression. This study investigated Nuclear Receptor Subfamily 1 Group D Member 1 (NR1D1) as a potential therapeutic target for modulating autophagy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!