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Gene therapy for epilepsy targeting neuropeptide Y and its Y2 receptor to dentate gyrus granule cells.
EMBO Rep
October 2024
Division of Neuroscience, IRCCS San Raffaele Scientific Institute, 20132, Milan, Italy.
Gene therapy is emerging as an alternative option for individuals with drug-resistant focal epilepsy. Here, we explore the potential of a novel gene therapy based on Neuropeptide Y (NPY), a well-known endogenous anticonvulsant. We develop a lentiviral vector co-expressing NPY with its inhibitory receptor Y2 in which, for the first time, both transgenes are placed under the control of the minimal CamKIIa(0.
View Article and Find Full Text PDFMisprogramming of glucose metabolism impairs recovery of hippocampal slices from neuronal GLT-1 knockout mice and contributes to excitotoxic injury through mitochondrial superoxide production.
J Neurochem
January 2025
Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
We have previously reported a failure of recovery of synaptic function in the CA1 region of acute hippocampal slices from mice with a conditional neuronal knockout (KO) of GLT-1 (EAAT2, Slc1A2) driven by synapsin-Cre (synGLT-1 KO). The failure of recovery of synaptic function is due to excitotoxic injury. We hypothesized that changes in mitochondrial metabolism contribute to the heightened vulnerability to excitotoxicity in the synGLT-1 KO mice.
View Article and Find Full Text PDFSex-dependent changes in AMPAR expression and Na, K-ATPase activity in the cerebellum and hippocampus of α-Klotho-Hypomorphic mice.
Neuropharmacology
November 2024
Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-900, São Paulo, SP, Brazil. Electronic address:
Aging is characterized by a functional decline in several physiological systems. α-Klotho-hypomorphic mice (Kl) exhibit accelerated aging and cognitive decline. We evaluated whether male and female α-Klotho-hypomorphic mice show changes in the expression of synaptic proteins, N-methyl-d-aspartate receptor (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits, postsynaptic density protein 95 (PSD-95), synaptophysin and synapsin, and the activity of Na, K-ATPase (NaK) isoforms in the cerebellum and hippocampus.
View Article and Find Full Text PDFPreclinical studies of gene replacement therapy for CDKL5 deficiency disorder.
Mol Ther
October 2024
PTC Therapeutics, Inc, 500 Warren Corporate Center Drive, Warren, NJ 07059, USA. Electronic address:
Article Synopsis
- - CDD is a rare neurodevelopmental disorder linked to mutations in the CDKL5 gene, leading to symptoms like epilepsy, muscle weakness, and developmental delays.
- - Researchers created a gene therapy vector, AAV9.Syn.hCDKL5, to deliver the CDKL5 gene to the brain, using a specific promoter to enhance gene expression.
- - Studies in mice showed that injecting the vector directly into the cerebrospinal fluid improved distribution and resulted in biological activity, with successful functional improvements observed at higher doses.
Overlapping role of synaptophysin and synaptogyrin family proteins in determining the small size of synaptic vesicles.
Proc Natl Acad Sci U S A
July 2024
Department of Neuroscience, Yale University School of Medicine, New Haven, CT 06510.
Members of the synaptophysin and synaptogyrin family are vesicle proteins with four transmembrane domains. In spite of their abundance in synaptic vesicle (SV) membranes, their role remains elusive and only mild defects at the cellular and organismal level are observed in mice lacking one or more family members. Here, we show that coexpression with synapsin in fibroblasts of each of the four brain-enriched members of this family-synaptophysin, synaptoporin, synaptogyrin 1, and synaptogyrin 3-is sufficient to generate clusters of small vesicles in the same size range of SVs.
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