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Linking altered neuronal and synaptic properties to nicotinic receptor Alpha5 subunit gene dysfunction: a translational investigation in rat mPFC and human cortical layer 6.
Transl Psychiatry
January 2025
Research Center Juelich, Institute of Neuroscience and Medicine 10, Research Center Juelich, Juelich, Germany.
Genetic variation in the α5 nicotinic acetylcholine receptor (nAChR) subunit of mice results in behavioral deficits linked to the prefrontal cortex (PFC). rs16969968 is the primary Single Nucleotide Polymorphism (SNP) in CHRNA5 strongly associated with nicotine dependence and schizophrenia in humans. We performed single cell-electrophysiology combined with morphological reconstructions on layer 6 (L6) excitatory neurons in the medial PFC (mPFC) of wild type (WT) rats, rats carrying the human coding polymorphism rs16969968 in Chrna5 and α5 knockout (KO) rats.
View Article and Find Full Text PDFDietary deacetylated chitin nanoparticles confer protection against diazinon toxicity in male African catfish: evaluation of immune-biochemical, antioxidant, and reproductive profiles.
Fish Physiol Biochem
January 2025
Fish Disease Department, Faculty of Veterinary Medicine, Aswan University, Aswan, 81528, Egypt.
Currently, deacetylated chitin (chitosan) nanoparticles (CNPs) are successfully utilized in aquaculture practices. This trial demonstrates the efficacy of CNPs in combating diazinon (DZN) toxicity in African catfish, Clarias gariepinus, via monitoring hepato-renal function, serum immune trait, hormonal function, and hepato-renal antioxidant activity. Four groups were allocated as follows: a control group, a CNPs group (0.
View Article and Find Full Text PDFImino and Thioureidic Derivatives as New Tools for Alzheimer's Disease: Preliminary Studies.
Chem Biol Drug Des
January 2025
Department of Health Sciences, University of Basilicata, Potenza, Italy.
Alzheimer's disease is a neurodegenerative chronic disease with a severe social and economic impact in the societies, which still lacks an efficient therapy. Several pathophysiological events (β-amyloid [Aβ] deposits, τ-protein aggregation, loss of cholinergic activity, and oxidative stress) occurs in the progression of the disease. Therefore, the search for efficient multi-targeted agents for the treatment of Alzheimer's disease becomes indispensable.
View Article and Find Full Text PDFIntegrating epigenetic modification and stem cell therapy strategies: A novel approach for advancing Alzheimer's disease treatment - A literature review.
Narra J
December 2024
Department of Histology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
Alzheimer's disease (AD) is the most frequent form of dementia and represents an increasing global burden, particularly in countries like Indonesia, where the population has begun to age significantly. Current medications, including cholinesterase inhibitors and NMDA receptor antagonists, have modest effects on clinical symptoms in the early to middle stages, but there is no curative treatment available so far despite progress. Activating or repressing epigenetic modifications, including DNA methylation, histone modification and microRNA regulation, appears to play an important role in AD development.
View Article and Find Full Text PDFMechanistic insight into neuroprotective effect of standardized ginger chemo varieties from Manipur, India in scopolamine induced learning and memory impaired mice.
Metab Brain Dis
January 2025
School of Natural Product Studies, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700 032, India.
Alzheimer's disease is a complex neurodegenerative disease characterized by progressive decline in cognitive function and behaviour. Ginger is the rhizome of the plant Zingiber officinale Roscoe, has been an important ingredient of many Ayurveda formulations to treat neurological disorders. The present study aims to estimate the variation of 6-gingerol content in nine different ginger samples collected from Manipur, India, investigate the neuroprotective potential of the most potent ginger sample against scopolamine-induced cognitively impaired mice, and validate the therapeutic claim by molecular docking analysis.
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