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Related Experiment Video

Updated: Jun 26, 2026

Using Live&#45;Cell Imaging to Measure the Effects of Pathological Proteins on Axonal Transport in Primary Hippocampal Neurons
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Using Live-Cell Imaging to Measure the Effects of Pathological Proteins on Axonal Transport in Primary Hippocampal Neurons

Published on: December 22, 2023

Compensatory Intercellular Mitochondrial Transfer Improves Bioenergetics in P301L Tau-Affected Neuronal Cells.

Aurélien Riou1,2, Aline Broeglin1,2, Andreas Papassotiropoulos2

  • 1Cell Biology & Energy Metabolism, University Psychiatric Clinics (UPK) Basel, University of Basel, 4002 Basel, Switzerland.

Cells
|June 25, 2026
PubMed
Summary
This summary is machine-generated.

Intercellular mitochondrial transfer (IMT) is enhanced in tauopathies, where abnormal tau protein drives this process. This transfer supports neuronal energy needs, offering potential therapeutic strategies for neurodegenerative diseases.

Keywords:
astrocytesintercellular mitochondrial transfermitochondrianeuronstauopathies

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Tauopathies involve abnormal tau protein accumulation, causing mitochondrial dysfunction and neuronal vulnerability due to high energy demands.
  • Intercellular mitochondrial transfer (IMT) is a mechanism where cells exchange mitochondria to support energy-deficient cells.

Purpose of the Study:

  • To investigate if intercellular mitochondrial transfer (IMT) is altered in tauopathies.
  • To determine the influence of abnormal tau protein on IMT between astrocytes and neurons.

Main Methods:

  • Utilized co-cultures of neuronal (SH-SY5Y) and astrocytic (A172) cell models.
  • Confirmed findings in human induced pluripotent stem cell (iPSC)-derived neurons and astrocytes.
  • Investigated IMT mechanisms and the fate of transferred mitochondria.

Main Results:

  • Intercellular mitochondrial transfer (IMT) is enhanced in the presence of abnormal tau.
  • IMT occurs primarily through contact-dependent mechanisms.
  • Transferred mitochondria were integrated, degraded, or remained isolated, improving cellular respiration and bioenergetics in pathological cells.

Conclusions:

  • Enhanced IMT in tauopathies represents an endogenous metabolic adaptation to mitigate neuronal energy deficits.
  • IMT highlights a link between tau pathology and neuronal metabolic adaptation.
  • IMT holds therapeutic potential for neurodegenerative diseases.