Neurons protect themselves from degeneration by adapting their metabolism, a study reveals

Neurons can counteract degeneration and promote survival by adapting their metabolism, revealed a recent study by researches at Karolinska Institute and Max Plank Institute. It challenges the well-established view that the neurons cannot adjust their metabolism and therefore irreversibly degenerate.

The defense mechanism prevents the degeneration of neurons. This helps to widen the therapeutic response of patients with mitochondrial dysfunction and Parkinson’s disease.

Neuronal degeneration pathology:

Mitochondria are membrane-bound cell organelles. They provide energy for the normal function of tissues in our body. Mitochondria is responsible for the activity of nerve cells. This mitochondrial dysfunction of the body opposes Parkinson’s disease, different ataxias, and several peripheral neuropathies.

Despite making attempts to prevent degeneration, a study on neuronal death caused by mitochondrial dysfunction’s limited.

Neurons are considered to be terminally differentiated cells. They have limited or no capacity to produce energy in challenging environments. There is enough proof which reveals that some neurological diseases can tolerate mitochondrial dysfunction for a lengthy period. A question which read whether degenerating neurons may activate a program of metabolic resilience was raised by the researchers.

Nils-Göran Larsson, the corresponding author of the study and professor at the Department of Medical Biochemistry and Biophysics at Karolinska Institute said, “We devised an innovative approach to purify degenerating neurons from the mouse brain and to analyze the global protein content, the proteome, of these neurons. Unexpectedly, the proteomic data showed the existence of a precisely coordinated, neuron-specific metabolic program that becomes activated in response to mitochondrial dysfunction”.


Metabolic rewiring makes neurons resistant to degeneration:

A form of metabolic rewiring makes neurons resistant to rapid generation, reports revealed. This metabolic adaption was thought to occur in external tissues or supporting cells in the brain. The ability of neurons to induce anaplerosis denotes its protective role. Neurons died at a much faster pace when anaplerosis was blocked. As a result, the disease became more severe.

The identification of metabolic rewiring in dysfunctional neurons gives hope to authors for developing the therapeutic approach to prolong neuronal survival and improve functions in patient with mitochondrial dysfunction and other types of neurodegeneration.

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