Researchers from King’s College London have made an important discovery about how different parts of nerve cells (neurons) age.
This finding could help in early detection of neurodegenerative diseases like ALS (amyotrophic lateral sclerosis) and Alzheimer’s disease (AD).
Their study was published in the journal Aging Cell.
Neurons are special cells that send and receive information from the brain and communicate with the rest of the body. Unlike other cells, neurons do not replicate, so they need other ways to stay healthy.
One way is through mitochondrial trafficking. Mitochondria, the parts of the cell that make energy, are transported from the central body of the neuron (called the soma) to its axon, which is a long tail-like structure that sends signals to other cells.
As we age, the movement of mitochondria slows down, especially in neurodegenerative diseases, and this slowdown can signal further brain degeneration.
Until now, it wasn’t clear how the decline in mitochondrial transport and function during aging were connected.
To investigate, the researchers used a technique involving fluorescence to measure the thickness (viscosity) of the fluid inside neurons in mice.
They found that as the mice aged, the fluid in the soma became thicker, but the fluid in the axon did not. This increased viscosity in the soma seems to trap the mitochondria, preventing them from moving to the axon and affecting the neuron’s health.
The researchers believe that by comparing the viscosity of the fluid inside neurons in healthy individuals of similar age, they could use changes in viscosity as an early warning sign for neurodegenerative diseases in the future.
Dr. Alessio Vagnoni, the lead author of the study, explained, “The movement of cellular components like mitochondria is crucial for a healthy neuron.
Essentially, movement is life and stillness is death. By understanding how the viscosity changes in neurons as they age, we can identify potential targets for new drugs and treatments.”
This research also opens the door to mapping specific neurodegenerative diseases to changes in cytoplasmic viscosity, adding new biomarkers for these illnesses. Ultimately, this could improve drug treatments by providing a more complete picture of the target areas within neurons.
The team hopes to continue studying how environmental factors and additional illnesses might impact the fluid inside neurons as they age, potentially leading to neurodegeneration. This work could lead to new ways of detecting and treating neurodegenerative diseases early, improving the quality of life for many people.
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