The purpose of this study is to investigate the change of the whole brain event-related potentials(P300) in normal brain aging based on N-back cognitive tasks. The P300 of 15 normal young people and 10 normal old people were evaluated based on N-back cognitive tasks and analyzed. The results showed that the P300 latency of old people was longer in whole brain than young people, and amplitude was increased in the frontal-central region, while significantly increased in the pre-frontal region in the same load cognitive tasks. With the cognitive task load increasing, the amplitude of old people in high-load task was higher in the whole brain than that in low-load task, mainly in in the frontal region, but the difference was not statistically significant. The latency in the high-load task was shorter in the frontal-central region of right brain than the low-load task, and the difference was statistically significant. Thus, P300 showed that the normal brain aging process is mainly reflected in the pre-frontal region, and the high-load cognitive task could better reflect the change of brain function compared with the low-load cognitive task. The finding is of revelatory meaning for diagnosis of early dementia in patients.
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http://dx.doi.org/10.7507/1001-5515.201704031 | DOI Listing |
BMC Pharmacol Toxicol
January 2025
Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, 240003, Nigeria.
Background: Glia mediated neuroinflammation and degeneration of inhibitory GABAergic interneurons are some of the hall marks of pyrethroid neurotoxicity. Here we investigated the sex specific responses of inflammatory cytokines, microglia, astrocyte and parvalbumin positive inhibitory GABAergic interneurons to λ-cyhalothrin (LCT) exposures in rats.
Methods: Equal numbers of male and female rats were given oral corn oil, 2 mg/kg.
Mol Neurodegener
January 2025
The Picower Institute for Learning and Memory, Cambridge, MA, USA.
Many diseases and disorders of the nervous system suffer from a lack of adequate therapeutics to halt or slow disease progression, and to this day, no cure exists for any of the fatal neurodegenerative diseases. In part this is due to the incredible diversity of cell types that comprise the brain, knowledge gaps in understanding basic mechanisms of disease, as well as a lack of reliable strategies for delivering new therapeutic modalities to affected areas. With the advent of single cell genomics, it is now possible to interrogate the molecular characteristics of diverse cell populations and their alterations in diseased states.
View Article and Find Full Text PDFSci Rep
January 2025
Support Centre for Advanced Neuroimaging (SCAN), Institute for Diagnostic and Interventional Neuroradiology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
This study aims to establish an imitation task of multi-finger haptics in the context of regular grasping and regrasping processes during activities of daily living. A video guided the 26 healthy, right-handed volunteers through the three phases of the task: (1) fixation of a hand holding a cuboid, (2) observation of the sensori-motor manipulation, (3) imitation of that motor action. fMRI recorded the task; graph analysis of the acquisitions revealed the associated functional cerebral connectivity patterns.
View Article and Find Full Text PDFJ Mol Histol
January 2025
Clinical Pharmacology Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt.
Type 2 diabetes mellitus (T2DM) adversely affects various organs, including the brain and its blood barrier. In addition to the brain, hyperglycemia damages the testes. The testes possess blood-tissue barriers that share common characteristics and proteins with the blood-brain barrier (BBB), including breast cancer-resistant protein (BCRP).
View Article and Find Full Text PDFNature
January 2025
Institute of Molecular Health Sciences, Department of Biology, Swiss Federal Institute of Technology (ETH) Zurich, Zurich, Switzerland.
During normal cellular homeostasis, unfolded and mislocalized proteins are recognized and removed, preventing the build-up of toxic byproducts. When protein homeostasis is perturbed during ageing, neurodegeneration or cellular stress, proteins can accumulate several forms of chemical damage through reactive metabolites. Such modifications have been proposed to trigger the selective removal of chemically marked proteins; however, identifying modifications that are sufficient to induce protein degradation has remained challenging.
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