The mouse model of Alzheimer's disease (AD), Tg2576 mice (APP), has provided valuable information, such as the role of the metallothionein (MT) family in their behavioral and amyloidosis phenotypes. In this study, we further characterize the role of MT-1 by crossing -overexpressing mice with Tg2576 mice (APPTgMT). In 14-month-old mice, MT-1(/2) protein levels were dramatically increased by overexpression throughout the cortex (Cx), which showed a prominent caudal-rostral gradient, and the hippocampus (HC). There was a trend for MT-1(/2) immunostaining to be increased in the areas surrounding the amyloid plaques in control male mice but not in -overexpressing mice. Gliosis was elicited by the amyloid plaques, but the effects of overexpression were modest. However, in hippocampal western blots the microglial marker Iba-1 was increased in old male APPTgMT mice compared to APP-wild type (APPWT) mice, and the opposite was observed in young mice. Hippocampal CA1 neuronal loss was observed in Tg2576 mice, but was unaffected by overexpression. Aging increased Zn and Cu levels differently depending on brain area, sex, and genotype. Thus, the effects of overexpression on the phenotype of Tg2576 mice here studied are modest.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343787 | PMC |
http://dx.doi.org/10.3390/ijms18020251 | DOI Listing |
Mol Med
December 2024
Department of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, 42 Jaebong-Ro, Dong-Gu, Gwangju, 61469, Republic of Korea.
Background: Recent studies have identified hearing loss (HL) as a primary risk factor for Alzheimer's disease (AD) onset. However, the mechanisms linking HL to AD are not fully understood. This study explored the effects of drug-induced hearing loss (DIHL) on the expression of proteins associated with AD progression in mouse models.
View Article and Find Full Text PDFPhysiol Behav
December 2024
Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Deptment of Neuroscience & Regenerative Medicine, Augusta, GA 30912, USA; College of Agriculture, Food, and Natural Resources, Prairie View A&M University, Prairie View, TX 77446, USA; Centre for Healthy Aging, Medical College of Georgia, Augusta University, Augusta, GA, USA; Department of Cell Biology and Anatomy, Medical College of Georgia, Augusta University, GA, USA; Department of Orthopedic Surgery, Medical College of Georgia, Augusta University, Augusta, GA, USA. Electronic address:
Alzheimer's Disease (AD) is a debilitating neurocognitive disorder with an unclear underlying mechanism. Recent studies have implicated gut microbiota dysbiosis with the onset and progression of AD. The connection between gut microbiota and AD can significantly affect the prevention and treatment of AD patients.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, 04100 Latina, Italy.
Endocannabinoids have attracted great interest for their ability to counteract the neuroinflammation underlying Alzheimer's disease (AD). Our study aimed at evaluating whether this activity was also due to a rebalance of autophagic mechanisms in cellular and animal models of AD. We supplied URB597, an inhibitor of Fatty-Acid Amide Hydrolase (FAAH), the degradation enzyme of anandamide, to microglial cultures treated with Aβ, and to Tg2576 transgenic mice, thus increasing the endocannabinoid tone.
View Article and Find Full Text PDFJ Neurochem
November 2024
Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.
Extra-cerebral manifestations of Alzheimer's disease (AD) develop in the retina, which is, therefore, considered a "window to the brain". Recent studies demonstrated the dysregulation of the endocannabinoid (eCB) system (ECS) in AD brain. Here, we explored the possible alterations of ECS and the onset of gliosis in the retina of AD-like mice.
View Article and Find Full Text PDFSleep Med
December 2024
Department of Neurology, University Hospital Zurich (USZ), Switzerland; Neuroscience Center Zurich (ZNZ), Switzerland; Center of Competence Sleep and Health, University of Zurich (UZH), Switzerland. Electronic address:
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!