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Basic Science and Pathogenesis.

André Nunes Mensch1, Giovanna Carello-Collar2, Vanessa Gomes Ramos1

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Autosomal dominant Alzheimer's disease (ADAD) mutations disrupt normal gene expression correlations in developing rat brains, suggesting early synaptic dysfunction. These findings highlight critical neurodevelopmental changes in ADAD embryos.

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Area of Science:

  • Neuroscience
  • Genetics
  • Developmental Biology

Background:

  • Alzheimer's disease (AD) is linked to altered neuronal plasticity, excitatory/inhibitory imbalance, and neuroinflammation.
  • Autosomal dominant Alzheimer's disease (ADAD) mutations cause early neuronal connectivity changes, indicating a potential neurodevelopmental origin.
  • The precise developmental stage of dysfunction in inhibitory neurons and glial cells in ADAD remains unclear.

Purpose of the Study:

  • To investigate gene expression of inhibitory interneurons, astrocytes, and microglia during neurodevelopment in an ADAD rat model.
  • To identify early molecular markers of ADAD-related neurodevelopmental alterations.

Main Methods:

  • Gene expression of parvalbvalbumin (Pvalb), somatostatin (Sst), Slc1a3, glial fibrillary acidic protein (Gfap), and integrin subunit alpha M (Itgam) was quantified using RT-qPCR in wild-type (WT) and TgF344-AD (TG) rat embryos at gestational day 13.5.
  • Statistical comparisons and correlation analyses (Pearson Correlation, linear regression) were performed between WT and TG groups.

Main Results:

  • No significant differences in the expression levels of individual genes (Pvalb, Sst, Slc1a3, Gfap, Itgam) were found between WT and ADAD embryos.
  • Significant correlations between gene pairs (Pvalb-Itgam, Sst-Slc1a3, Slc1a3-Gfap) were observed in WT embryos but were absent in ADAD embryos.
  • Absence of these gene expression correlations in ADAD embryos suggests early disruptions in neural circuitry.

Conclusions:

  • The study reveals that ADAD mutations abolish specific gene expression correlations during early neurodevelopment, indicating potential synaptic dysfunction.
  • These findings suggest that ADAD-related neurodevelopmental alterations occur earlier than previously thought.
  • Further research at later gestational stages is needed to fully elucidate the impact of ADAD mutations on the inhibitory neuron-microglia interplay.