Introduction: Higher brain tocopherol levels have been associated with lower levels of Alzheimer's disease (AD) neuropathology; however, the underlying mechanisms are unclear.
Methods: We studied the relations of α- and γ-tocopherol brain levels to microglia density in 113 deceased participants from the Memory and Aging Project. We used linear regression analyses to examine associations between tocopherol levels and microglia densities in a basic model adjusted for age, sex, education, apolipoprotein E ()ε4 genotype (any ε4 allele vs. none) , and post-mortem time interval, and a second model additionally adjusted for total amyloid load and neurofibrillary tangle severity.
Results: Higher α- and γ-tocopherol levels were associated with lower total and activated microglia density in cortical but not in subcortical brain regions. The association between cortical α-tocopherol and total microglia density remained statistically significant after adjusting for AD neuropathology.
Discussion: These results suggest that the relation between tocopherols and AD might be partly explained by the alleviating effects of tocopherols on microglia activation.
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http://dx.doi.org/10.1002/trc2.12021 | DOI Listing |
Int J Mol Sci
January 2025
Department of Functional Biochemistry of the Nervous System, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow 117485, Russia.
Traumatic brain injury (TBI) is one of the primary causes of mortality and disability, with arterial blood pressure being an important factor in the clinical management of TBI. Spontaneously hypertensive rats (SHRs), widely used as a model of essential hypertension and vascular dementia, demonstrate dysfunction of the hypothalamic-pituitary-adrenal axis, which may contribute to glucocorticoid-mediated hippocampal damage. The aim of this study was to assess acute post-TBI seizures, delayed mortality, and hippocampal pathology in SHRs and normotensive Sprague Dawley rats (SDRs).
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Division of Medical Sciences, University of Victoria, Victoria, BC, Canada.
The brain presents various structural and functional sex differences, for which multiple factors are attributed: genetic, epigenetic, metabolic, and hormonal. While biological sex is determined by both sex chromosomes and sex hormones, little is known about how these two factors interact to establish this dimorphism. Sex differences in the brain also affect its resident immune cells, microglia, which actively survey the brain parenchyma and interact with sex hormones throughout life.
View Article and Find Full Text PDFTzu Chi Med J
August 2024
Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Schizophrenia (SCZ) is a chronic psychotic disorder that profoundly alters an individual's perception of reality, resulting in abnormal behavior, cognitive deficits, thought distortions, and disorientation in emotions. Many complicated factors can lead to SCZ, and investigations are ongoing to understand the neurobiological underpinnings of this condition. Presynaptic Netrin G1 and its cognate partner postsynaptic Netrin-G-Ligand-1 (NGL-1) have been implicated in SCZ.
View Article and Find Full Text PDFAm J Nucl Med Mol Imaging
December 2024
Cyclotron and Radiochemistry Core, Karmanos Cancer Institute Detroit, MI, USA.
Colony-stimulating factor 1 receptor (CSF1R) is almost exclusively expressed on microglia in the human brain and thus, has promise as a biomarker for imaging microglia density as a proxy for neuroinflammation. [C]CPPC is a radiotracer with selective affinity to CSF1R, and has been evaluated for in-human microglia PET imaging. The flourine-18 labeled CPPC derivative, 5-cyano-N-(4-(4-(2-[F]fluoroethyl)piperazin-1-yl)-2-(piperidin-1-yl)phenyl)furan-2-carboxamide ([F]FCPPC), was previously synthesized, however, with a low radiochemical yield using manual radiosynthesis.
View Article and Find Full Text PDFInt J Eat Disord
January 2025
Institute of Anatomy, Rostock University Medical Center, Rostock, Germany.
Objective: Anorexia nervosa (AN) is an eating disorder characterized by severe weight loss and associated with hyperactivity and circadian rhythm disruption. However, the cellular basis of circadian rhythm disruption is poorly understood. Glial cells in the suprachiasmatic nucleus (SCN), the principal circadian pacemaker, are involved in regulating circadian rhythms.
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