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September 1, 2020 /--- In a recent study, scientists found that the absence of AMPK, an important energy regulator in neurostar-shaped glial cells, causes neuronal death, which in turn leads to spontaneous brain seizures in animals.
team, led by Cincinnati pediatric cancer biologist Dr. Biplab Dasgupta, published their findings in the journal Cell Reports.
results show that the absence of AMPK in astrological glial cells can lead to severe damage to glucose and lactic acid metabolism in neurons.
study, conducted by Dr. Raghu Rao of UM and Dr Ivan Tkac of UM, found that lactic acid levels in mice missing from AMPK decreased by about 40.
missing neurons in AMPK indicate spontaneous seizures and are susceptible to small doses of seizure inducers.
anti-diabetic drug metformin activates AMPK) may reduce seizures.
lead researcher at the Institute of Cancer and Hematology, said metformin is currently being preclinically tested in rodents.
Dasgupta said: "Little is known about how astrological glial cells regulate glycolysis to produce lactic acid and provide it to neurons to support their metabolism and normal functioning.
the first time that AMP kinase (AMPK) is the key to controlling the mechanisms of astrogenic cell saccharin and lactic acid production in the brain.
and we have shown that interfering with this process does little damage to astrological glial cells, but damages neurons.
, co-author of the study and a professor at the University of Mist in Germany, found that the absence of AMPK in glial cells in goesflies can lead to neuron death and shorten the lifespan of mutant fruit flies.
researchers say this and other results, including retaining these functions in human astrological glial cells, make it possible for AMPK-controlled lactic acid metabolism to support human neurons.
(bioon.com) Source: Scientists discover key regulator of neuron function and survival Original source: Ranjithmenon Muraleedharan et al, AMPK-Regulatory astrocytic Lactate Shuttle Plays a Non-Cell-Autonomous Role in Neuronal Survival, Cell Reports (2020). DOI: 10.1016/j.celrep.2020.108092.