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In utero Electroporation followed by Primary Neuronal Culture for Studying Gene Function in Subset of Cortical Neurons

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Transcriptomic alterations in APP/PS1 mice astrocytes lead to early postnatal axon initial segment structural

María José Benitez^1,2, Diana Retana¹, Lara Ordoñez-Gutiérrez^3,4

¹Instituto Cajal, CSIC, Madrid, Spain.

Cellular and Molecular Life Sciences : CMLS

|November 1, 2024

Summary

Early Alzheimer's disease (AD) changes involve astrocyte alterations affecting the axon initial segment (AIS). This study reveals glial cells impact neuronal function, offering new therapeutic targets for AD.

Keywords:

ADNP AnkyrinG Astrocytes Axon initial segment Neurodegeneration P2X7 Retinoic acid

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Area of Science:

Neuroscience
Cell Biology
Neurodegenerative Diseases

Background:

Alzheimer's disease (AD) involves neuronal dysfunction and degeneration.
The axon initial segment (AIS) is critical for neuronal function, and its alterations are observed in AD.
The glial contribution to AIS deregulation in AD remains unclear.

Purpose of the Study:

To investigate early postnatal AIS mechanisms in wild-type and APP/PS1 mice.
To explore the role of astrocytes in AIS modulation in the context of AD.
To identify potential therapeutic targets for preventing AIS dysfunction in AD.

Main Methods:

Comparative analysis of AIS in wild-type and APP/PS1 mice from postnatal day 21 (P21).
Neuron-astrocyte co-culture experiments to assess astrocyte influence on AIS.
Molecular analysis of retinoic acid synthesis enzymes, ADNP, and P2X7 receptor pathways.
In vivo treatment with P2X7 inhibitors in APP/PS1 mice.

Main Results:

APP/PS1 mice exhibited AIS integrity loss, reduced ankyrinG expression, and AIS shortening from P21.
APP/PS1 astrocytes induced AIS integrity loss in wild-type neurons.
Reduced expression of retinoic acid synthesis enzymes (Rdh1, Aldh1b1) and ADNP in APP/PS1 astrocytes contributed to AIS changes.
AIS integrity in wild-type neurons was restored by inhibiting retinoic acid degradation, adding NAP peptide, or inhibiting P2X7 receptors.
Long-term P2X7 inhibitor treatment ameliorated AIS disruption in APP/PS1 mice.

Conclusions:

Astrocytes play a significant role in modulating AIS integrity early in postnatal development.
Alterations in astrocytes, including reduced ADNP and altered retinoic acid signaling, can lead to AIS dysfunction.
Targeting glial cell pathways, such as P2X7 receptors, may offer novel therapeutic strategies for early AD intervention.