Scientists have found that the VAP protein stabilizes mitochondria in ALS

When we encounter new experiences, our neurons undergo rapid remodeling for learning, known as synaptic plasticity. Mitochondria, acting like biological batteries, support this energy-demanding process. Mitochondria are strategically anchored near synaptic sites for efficient energy delivery. However, the mechanism behind this anchoring was previously unknown.

Scientists at the Max Planck ID VAP have identified a molecular anchor that stabilizes mitochondria near synapses, which is important for memory. VAP mutation linked to ALS reveals potential ALS research avenues. Published in Nature Communications.

Dr. Vidya Rangaraju, lead scientist on the work and research team leader at the Max Planck Florida Institute, explains. Impacts, „We began this study to understand the fundamental properties of how memories work, and our findings open up important new directions for our research. We investigate the cellular mechanisms of cognitive symptoms that often occur alongside motor symptoms in ALS, but are not rigorously understood. The tools and approaches we have established will begin to shed light on this area.” We believe that.

Stable mitochondria near synapses support dendritic synaptic plasticity, which is critical for memory formation. Unlike axons, dendrites uniquely anchor mitochondria for local stability, ensuring efficient energy delivery during structural and functional changes.

The team chemically tagged extracellular mitochondrial proteins using a tool to detect proteins that anchor dendritic mitochondria, revealing more than 100 candidates. Focusing on those that interact with the actin cytoskeleton, important for synaptic structure, they identified a few. Genetic ablation of these candidates showed their important role in stabilizing mitochondria in dendrites.

ALS-associated VAP protein stabilizes mitochondria, which supports synaptic plasticity. Removal of VAP disrupts mitochondria-actin interactions, contractility, and dendritic mitochondria. Without VAP, mitochondria move away from synapses, affecting structural changes in synaptic plasticity during memory formation.

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The discovery of VAP as a mitochondrial anchor with roles in memory has implications for ALS research. A VAP mutation causes familial ALS, suggesting links between mitochondrial stability, energy support, and disease pathology. Driven by this discovery, researchers aim to investigate disruptions in brain function due to altered mitochondrial energy in ALS and other neurological disorders.

In conclusion, the scientists establish VAP as an important mitochondrial stabilizer linked to ALS, opening new avenues of research.

Journal Note:

  1. Babbat, O., Burimetla, D., Kruessel, S. and many others. VAP locally spatially stabilizes dendritic mitochondria to support synaptic plasticity. Natural communication. DOI: 10.1038/s41467-023-44233-8.

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