Adipose-derived stem cells protect motor neurons and reduce glial activation in both in vitro and in vivo models of ALS.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative condition for which new therapeutic options are urgently needed. We injected GFP + adipose-derived stem cells (EGFP-ADSCs) directly into the cerebrospinal fluid (CSF) of transgenic SOD1 G93A mice, a well-characterized model of familial ALS. Despite short-term survival of the injected cells and limited engraftment efficiency, EGFP-ADSCs improved motor function and delayed disease onset by promoting motor neuron (MN) survival and reducing glial activation. We then tested the in vitro neuroprotective potential of mouse ADSCs in astrocyte/MN co-cultures where ALS astrocytes show neurotoxicity. ADSCs were able to rescue MN death caused by ALS astrocytes derived from symptomatic SOD1 G93A mice. Further, ADSCs were found to reduce the inflammatory signature of ALS astrocytes by inhibiting the release of pro-inflammatory mediators and inducing the secretion of neuroprotective factors. Finally, mouse ADSCs were able to protect MNs from the neurotoxicity mediated by human induced astrocytes (iAstrocytes) derived from patients with either sporadic or familial ALS, thus for the first time showing the potential therapeutic translation of ADSCs across the spectrum of human ALS. These data in two translational models of ALS show that, through paracrine mechanisms, ADSCs support MN survival and modulate the toxic microenvir

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.