Mecp2 Deficiency in Peripheral Sensory Neuron Improves Cognitive Function by Enhancing Hippocampal Dendritic Spine Densities in Mice DOI Creative Commons
Yuting Feng,

Jingge Wang,

Jun Liu

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(11), P. 988 - 988

Published: June 6, 2024

Methyl-CpG-binding protein 2 (Mecp2) is an epigenetic modulator and numerous studies have explored its impact on the central nervous system manifestations. However, little attention has been given to potential contributions peripheral (PNS). To investigate regulation of Mecp2 in PNS specific regions, we generated Mecp2fl/flAdvillincre mice with sensory-neuron-specific deletion gene found mutant had a heightened sensitivity temperature, which, however, did not affect sense motion, social behaviors, anxiety-like behavior. Notably, comparison Mecp2fl/fl mice, exhibited improved learning memory abilities. The levels hippocampal synaptophysin PSD95 proteins were higher than mice. Golgi staining revealed significant increase total spine density, dendritic arborization pyramidal neurons compared In addition, activation BDNF-TrkB-CREB1 pathway was observed hippocampus spinal cord Intriguingly, BDNF/CREB1 signaling initiated within 5 days after birth. Our findings suggest therapeutic strategy targeting somasensory treat cognitive deficits associated disorders.

Language: Английский

Abnormal protein post-translational modifications induces aggregation and abnormal deposition of protein, mediating neurodegenerative diseases DOI Creative Commons
Wei Li, Honglian Li,

Jian‐Zhi Wang

et al.

Cell & Bioscience, Journal Year: 2024, Volume and Issue: 14(1)

Published: Feb. 12, 2024

Abstract Protein post-translational modifications (PPTMs) refer to a series of chemical that occur after the synthesis protein. Proteins undergo different such as phosphorylation, acetylation, ubiquitination, and so on. These can alter protein’s structure, function, interaction, thereby regulating its biological activity. In neurodegenerative diseases, several proteins abnormal modifications, which leads aggregation deposition protein, thus resulting in neuronal death related diseases. For example, main pathological features Alzheimer’s disease are beta-amyloid protein phosphorylation tau The ubiquitination loss α-synuclein onset Parkinson’s disease. Other diseases Huntington’s disease, amyotrophic lateral sclerosis, on also connected with PPTMs. Therefore, studying PPTMs is critical for understanding mechanism these development significant therapeutic strategies. This work reviews implications discusses relevant

Language: Английский

Citations

9
Immunotherapy in Alzheimer's Disease: From the Bench to the Bedside DOI
Breno S. Diniz

American Journal of Geriatric Psychiatry, Journal Year: 2024, Volume and Issue: 32(5), P. 584 - 585

Published: Jan. 14, 2024

Language: Английский

Citations

3
Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond DOI Creative Commons
Jenny Garmendia, Claudia Valentina De Sanctis, Viswanath Das

et al.

Current Neuropharmacology, Journal Year: 2023, Volume and Issue: 22(6), P. 1080 - 1109

Published: Oct. 19, 2023

Neurodegenerative disease (ND) incidence has recently increased due to improved life expectancy. Alzheimer's (AD) or Parkinson's (PD) are the most prevalent NDs. Both diseases poly genetic, multifactorial and heterogenous. Preventive medicine, a healthy diet, exercise, controlling comorbidities may delay onset. After diagnosed, therapy is needed slow progression. Recent studies show that local, peripheral age-related inflammation accelerates NDs' onset Patients with autoimmune disorders like inflammatory bowel (IBD) could be at higher risk of developing AD PD. However, no increase in ND been reported if patients adequately diagnosed treated. Autoantibodies against abnormal tau, β amyloid α- synuclein have encountered PD protective. This discovery led proposal immune-based therapies for involving monoclonal antibodies, immunization/ vaccines, pro-inflammatory cytokine inhibition anti-inflammatory addition. All different approaches analysed here. Future perspectives on new therapeutic strategies both concisely examined.

Language: Английский

Citations

6
Mecp2 Deficiency in Peripheral Sensory Neuron Improves Cognitive Function by Enhancing Hippocampal Dendritic Spine Densities in Mice DOI Creative Commons
Yuting Feng,

Jingge Wang,

Jun Liu

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(11), P. 988 - 988

Published: June 6, 2024

Methyl-CpG-binding protein 2 (Mecp2) is an epigenetic modulator and numerous studies have explored its impact on the central nervous system manifestations. However, little attention has been given to potential contributions peripheral (PNS). To investigate regulation of Mecp2 in PNS specific regions, we generated Mecp2fl/flAdvillincre mice with sensory-neuron-specific deletion gene found mutant had a heightened sensitivity temperature, which, however, did not affect sense motion, social behaviors, anxiety-like behavior. Notably, comparison Mecp2fl/fl mice, exhibited improved learning memory abilities. The levels hippocampal synaptophysin PSD95 proteins were higher than mice. Golgi staining revealed significant increase total spine density, dendritic arborization pyramidal neurons compared In addition, activation BDNF-TrkB-CREB1 pathway was observed hippocampus spinal cord Intriguingly, BDNF/CREB1 signaling initiated within 5 days after birth. Our findings suggest therapeutic strategy targeting somasensory treat cognitive deficits associated disorders.

Language: Английский

Citations

1