Microbiota–gut–brain axis in health and neurological disease: Interactions between gut microbiota and the nervous system

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(18)

Published: Sept. 1, 2024

Abstract Along with mounting evidence that gut microbiota and their metabolites migrate endogenously to distal organs, the ‘gut–lung axis,’ ‘gut–brain ‘gut–liver axis’ ‘gut–renal have been established. Multiple animal recent studies demonstrated may also be a key susceptibility factor for neurological disorders such as Alzheimer's disease, Parkinson's disease autism. The gastrointestinal tract is innervated by extrinsic sympathetic vagal nerves intrinsic enteric nervous system, interacts system maintain homeostatic balance in host gut. A total of 1507 publications on interactions between microbiota, gut–brain axis are retrieved from Web Science investigate underlying mechanisms involved normal states. We provide comprehensive overview effects its function neurotransmitter secretion, well alterations disorders, basis possibility targeting therapeutic agent disorders.

Language: Английский

---

AAV-mediated GBA1 and GDNF rescue neurological defects in a murine model of neuronopathic Gaucher disease

Molecular Therapy — Nucleic Acids, Journal Year: 2025, Volume and Issue: 36(2), P. 102506 - 102506

Published: March 7, 2025

Neuropathic Gaucher disease (nGD) is a life-threatening that progresses rapidly and caused by glucosylceramidase beta 1 (GBA1) mutation, which encodes the lysosomal hydrolase β-glucocerebrosidase (GCase). Nerve damage in nGD, associated with stunted growth development, arises from degeneration death of nervous system cells, often irreversible. Approved therapies effectively reduce substrate burden outside central (CNS) through augmenting mutant enzyme activity pharmacologic recombinant GCase or inhibiting glucocerebroside synthesis. However, these do not provide neuroprotection. In this study, we developed novel double-gene therapy based on adeno-associated virus (AAV), AAV9-GBA1-GDNF, stably expresses human GBA1 glial derived neurotrophic factor (GDNF) over long term. Pathological, molecular, proteomic tests nGD model confirmed early stages are characterized deficiency, loss neuronal function, even death. After treatment lifespan mice was extended, weight, brain motor ability were recovered. Additionally, GDNF additively prevented irreversible activating AKT/GSK3β pathway. These findings offer potential therapeutic strategies for other neurodegenerative diseases dysfunction.

Language: Английский

---

Alpha-Synuclein drives NURR1 and NLRP3 Inflammasome dysregulation in Parkinson's disease: From pathogenesis to potential therapeutic strategies

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 156, P. 114692 - 114692

Published: April 22, 2025

Language: Английский

---

CDNF overexpression prevents motor-cognitive dysfunction by intrastriatal CPP-based delivery system in a Parkinson's disease animal model

Neuropeptides, Journal Year: 2023, Volume and Issue: 102, P. 102385 - 102385

Published: Oct. 11, 2023

Language: Английский

---

Viral and nonviral approaches

Handbook of clinical neurology, Journal Year: 2024, Volume and Issue: unknown, P. 83 - 97

Published: Jan. 1, 2024

Language: Английский

---

Unlocking the promise of MANF in diseases: Mechanistic insights and therapeutic potentials

Molecular Biology Reports, Journal Year: 2024, Volume and Issue: 51(1)

Published: Nov. 16, 2024

Language: Английский

---

Cinnamaldehyde Attenuates the Expression of IBA1 and GFAP to Inhibit Glial Cell Activation and Inflammation in the MPTP‐Induced Acute Parkinson’s Disease Model

Parkinson s Disease, Journal Year: 2024, Volume and Issue: 2024(1)

Published: Jan. 1, 2024

Cinnamaldehyde (CA), the primary bioactive compound in cinnamon (

Language: Английский

---