Electroacupuncture remediates glial dysfunction and ameliorates neurodegeneration in the astrocytic α-synuclein mutant mouse model.

J Neuroinflammation

Departments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China.

Published: May 2015

AI Article Synopsis

  • The study explored the effects of electroacupuncture (EA) on neurodegenerative disease symptoms and neurochemical changes in a mouse model with a mutant α-synuclein protein.
  • EA improved motor function in mice exhibiting neuroinflammation and reduced the activation of harmful brain cells, while also protecting against the loss of important neurons.
  • The findings suggest EA could help treat motor abnormalities by promoting anti-inflammatory and antioxidant responses in the brain's affected areas.

Article Abstract

Background: The acupuncture or electroacupuncture (EA) shows the therapeutic effect on various neurodegenerative diseases. This effect was thought to be partially achieved by its ability to alleviate existing neuroinflammation and glial dysfunction. In this study, we systematically investigated the effect of EA on abnormal neurochemical changes and motor symptoms in a mouse neurodegenerative disease model.

Methods: The transgenic mouse which expresses a mutant α-synuclein (α-syn) protein, A53T α-syn, in brain astrocytic cells was used. These mice exhibit extensive neuroinflammatory and motor phenotypes of neurodegenerative disorders. In this study, the effects of EA on these phenotypic changes were examined in these mice.

Results: EA improved the movement detected in multiple motor tests in A53T mutant mice. At the cellular level, EA significantly reduced the activation of microglia and prevented the loss of dopaminergic neurons in the midbrain and motor neurons in the spinal cord. At the molecular level, EA suppressed the abnormal elevation of proinflammatory factors (tumor necrosis factor-α and interleukin-1β) in the striatum and midbrain of A53T mice. In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits).

Conclusions: These results suggest that EA possesses the ability to ameliorate mutant α-syn-induced motor abnormalities. This ability may be due to that EA enhances both anti-inflammatory and antioxidant activities and suppresses aberrant glial activation in the diseased sites of brains.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4449593PMC
http://dx.doi.org/10.1186/s12974-015-0302-zDOI Listing

Publication Analysis

Top Keywords

glial dysfunction
8
motor
5
electroacupuncture remediates
4
remediates glial
4
dysfunction ameliorates
4
ameliorates neurodegeneration
4
neurodegeneration astrocytic
4
astrocytic α-synuclein
4
mutant
4
α-synuclein mutant
4

Similar Publications

Neuroinflammation and mitochondrial dysfunction are early events in Alzheimer's disease (AD) and contribute to neurodegeneration and cognitive impairment. Evidence suggests that the inflammatory axis mediated by macrophage migration inhibitory factor (MIF) binding to its receptor, CD74, plays an important role in many central nervous system (CNS) disorders such as AD. Our group has developed DRhQ, a novel CD74 binding construct which competitively inhibits MIF binding, blocks macrophage activation and migration into the CNS, enhances anti-inflammatory microglia cell numbers and reduces pro-inflammatory gene expression.

View Article and Find Full Text PDF

We previously identified a role for dAuxilin (dAux), the fly homolog of Cyclin G-associated kinase, in glial autophagy contributing to Parkinson's disease (PD). To further dissect the mechanism, we present evidence here that lack of glial dAux enhanced the phosphorylation of the autophagy-related protein Atg9 at two newly identified threonine residues, T62 and T69. The enhanced Atg9 phosphorylation in the absence of dAux promotes autophagosome formation and Atg9 trafficking to the autophagosomes in glia.

View Article and Find Full Text PDF

Astrocytes are the primary cell type in the central nervous system, responsible for maintaining the stability of the brain's internal environment and supporting neuronal functions. Researches have demonstrated the close relationship between astrocytes and the pathophysiology and etiology of major depressive disorder. However, the regulatory mechanisms of astrocytes during depression remain unclear.

View Article and Find Full Text PDF

Remote photobiomodulation ameliorates behavioral and neuropathological outcomes in a rat model of repeated closed head injury.

Transl Psychiatry

January 2025

Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, Guangdong, China.

Repeated closed-head injuries (rCHI) from activities like contact sports, falls, military combat, and traffic accidents pose a serious risk due to their cumulative impact on the brain. Often, rCHI is not diagnosed until symptoms of irreversible brain damage appear, highlighting the need for preventive measures. This study assessed the prophylactic efficacy of remote photobiomodulation (PBM) targeted at the lungs against rCHI-induced brain injury and associated behavioral deficits.

View Article and Find Full Text PDF

Microglial polarization and ferroptosis are important pathological features in Alzheimer's disease (AD). Ghrelin, a brain-gut hormone, has potential neuroprotective effects in AD. This study aimed to explore the potential mechanisms by which ghrelin regulates the progression of AD, as well as the crosstalk between microglial polarization and ferroptosis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!