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Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their...
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Bone Marrow-Derived Mesenchymal Stem Cells and

Asmaa Gaber1, Ahlam M Elbakry1, Rabab M Aljarari2

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Mesenchymal stem cells (MSCs) and a gamma-secretase inhibitor (GSI-953) given to pregnant rats protected offspring from Alzheimer's-like neurodegeneration. These treatments reduced inflammation and improved brain development in newborns exposed to amyloid beta.

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Area of Science:

  • Neuroscience
  • Stem Cell Biology
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is a leading cause of neurodegeneration, characterized by amyloid beta (Aβ) plaques and hyperphosphorylated Tau (p-Tau).
  • AD disproportionately affects females, highlighting the need for sex-specific therapeutic evaluations.
  • Therapeutic interventions targeting AD pathology before significant cognitive decline offer a window of opportunity.

Purpose of the Study:

  • To evaluate the protective effects of bone marrow-derived mesenchymal stem cells (BM-MSCs) and gamma-secretase inhibitor-953 (GSI-953) on Aβ25-35-induced cognitive impairment and neurodegeneration.
  • To assess these treatments in a maternal-offspring model, examining effects on dams during pregnancy and their offspring's brain development.
  • To investigate the underlying mechanisms, including neuroinflammation, neurotrophic signaling, and gene expression changes.

Main Methods:

  • Rat dams were injected with Aβ25-35 to induce AD-like pathology prior to pregnancy.
  • Dams received intravenous BM-MSCs or oral GSI-953 during pregnancy.
  • Cognitive function was assessed using Y-maze and novel object recognition tests.
  • Offspring brains were analyzed for histology (dendritic morphology, microglial activation), neurochemistry (cytokines, APP, p-Tau, BDNF, GSK-3β), and gene expression.

Main Results:

  • Aβ25-35 injection impaired dam cognition and induced neuroinflammation and dendritic damage in offspring.
  • BM-MSC and GSI-953 treatments significantly improved offspring neurodevelopment, reducing microglial activation and increasing dendritic length.
  • Treatments reversed Aβ25-35-induced elevations in amyloid precursor protein (APP) and p-Tau, while increasing brain-derived neurotrophic factor (BDNF) and decreasing glycogen synthase kinase-3β (GSK-3β).
  • Offspring gene expression patterns were normalized, and overall newborn brain development disruptions were prevented.

Conclusions:

  • Maternal administration of BM-MSCs or GSI-953 provides broad-spectrum protection against Aβ25-35-induced neurodevelopmental deficits in offspring.
  • These treatments effectively suppress neuroinflammation, restore neural plasticity, and promote neurotrophic signaling.
  • The findings suggest a promising therapeutic strategy for mitigating Alzheimer's disease-related neurodegeneration, particularly considering the higher prevalence in females.