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GABA/Glutamate Neuron Differentiation Imbalance and Increased AKT/mTOR Signaling in CNTNAP2 Cerebral Organoids.
Biol Psychiatry Glob Open Sci
January 2025
Biomedical Research Institute, Foundation for Research and Technology-Hellas, University Campus, Ioannina, Greece.
Background: The polygenic nature of autism spectrum disorder (ASD) requires the identification of converging genetic pathways during early development to elucidate its complexity and varied manifestations.
Methods: We developed a human cerebral organoid model from induced pluripotent stem cells with targeted genome editing to abolish protein expression of the ASD risk gene.
Results: CNTNAP2 cerebral organoids displayed accelerated cell cycle, ventricular zone disorganization, and increased cortical folding.
Therapeutic Potential of DAAO Inhibitors for Cognitive Impairment Associated with Schizophrenia: Learnings from Luvadaxistat.
Int J Neuropsychopharmacol
January 2025
Neurocrine Biosciences, Inc., San Diego, CA.
Hypofunction of the N-methyl-D-aspartate receptor (NMDAR) has been proposed to underlie the pathophysiology of schizophrenia, suggesting that promoting NMDAR activity may alleviate the negative or cognitive symptoms associated with schizophrenia. To circumvent excitotoxicity that may accompany direct agonism of the glutamate binding site on the NMDAR, therapeutic trials have focused on targeting the glycine binding site on the NMDAR. Direct administration of either glycine or D-serine, both of which are endogenous coagonists at the NMDAR glycine site, has yielded mixed outcomes across an array of clinical trials investigating different doses or patient populations.
View Article and Find Full Text PDFChallenges of Investigating Compartmentalized Brain Energy Metabolism Using Nuclear Magnetic Resonance Spectroscopy in vivo.
Neurochem Res
January 2025
Department of Experimental Medical Science, Faculty of Medicine, Lund University, Lund, Sweden.
Brain function requires continuous energy supply. Thus, unraveling brain metabolic regulation is critical not only for our basic understanding of overall brain function, but also for the cellular basis of functional neuroimaging techniques. While it is known that brain energy metabolism is exquisitely compartmentalized between astrocytes and neurons, the metabolic and neuro-energetic basis of brain activity is far from fully understood.
View Article and Find Full Text PDFTau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation.
PLoS One
January 2025
Department of Anesthesiology & Perioperative Medicine, University of Rochester, Rochester, New York, United States of America.
Article Synopsis
- Neurodegenerative diseases like Alzheimer's are linked to problems with mitochondria, specifically mitophagy, which is the process of removing damaged mitochondria.
- Research indicates that mutated tau proteins can inhibit this process, affecting cell health during oxidative stress.
- In this study, it was found that certain tau mutations reduce levels of a key mitophagy receptor, FKBP8, which could help explain tau's role in mitochondrial dysfunction related to Alzheimer's and suggest FKBP8 as a target for future treatments.
Aerobic Exercise Improves Cognitive Recovery in Mice with Chronic Cerebral Hypoperfusion by Modulating the Annexin-A1-MAPK Axis and Astrocyte Polarization.
Aging Dis
December 2024
Central Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China.
Vascular cognitive impairment and dementia (VCID), resulting from chronic cerebral hypoperfusion, represent the second most prevalent form of dementia globally. Aerobic exercise is widely acknowledged as an effective intervention for various cognitive disorders. This study utilized a bilateral common carotid artery stenosis (BCAS) model to investigate whether aerobic exercise promotes cognitive recovery through the Annexin-A1 (ANXA1)/mitogen-activated protein kinase (MAPK) axis in BCAS mice.
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