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[[Key molecular pathways in ALS]] | [[Key molecular pathways in ALS]] | ||
| − | + | == Discussion threads on the ALSTDI forum == | |
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| + | [http://www.alstdi.org/forum/yaf_postst54840_sarm1-nad-and-neuroprotection.aspx SARM1 and neuroprotection (2015)]: | ||
| + | :''Moreover, they found that this protein, once unleashed, causes a rapid decline in the energy supply within axons. Within minutes after the protein - called SARM1 - is activated in neurons, a massive loss of nicotinamide adenine dinucleotide (NAD), a chemical central to a cell's energy production, occurs within the axon. "When a nerve is diseased or injured, SARM1 becomes more active, initiating a series of events that quickly causes an energetic catastrophe within the axon, and the axon undergoes self-destruction," said first author Josiah Gerdts, an MD/PhD student in Milbrandt's laboratory. Working in neurons in which SARM1 was activated, the researchers showed they could completely block axon degeneration and neuron cell death by supplementing the cells with a precursor to NAD, a chemical called nicotinamide riboside. The neurons were able to use nicotinamide riboside to keep the axons energized and healthy.'' | ||
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| + | [http://www.alstdi.org/forum/yaf_postst50386_scientists-identify-first-gene-in-programmed-axon-degeneration.aspx Scientists identify first gene in programmed axon degeneration (2012)]: | ||
| + | :''Degeneration of the axon and synapse, the slender projection through which neurons transmit electrical impulses to neighboring cells, is a hallmark of some of the most crippling neurodegenerative and brain diseases such as amyotrophic lateral sclerosis (ALS), Huntington's disease and peripheral neuropathy. Scientists have worked for decades to understand axonal degeneration and its relation to these diseases. Now, researchers at the University of Massachusetts Medical School are the first to describe a gene – dSarm/Sarm1 – responsible for actively promoting axon destruction after injury. The research, published today online by Science, provides evidence of an exciting new therapeutic target that could be used to delay or even stop axon decay.'' | ||
