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November 17, 2020 // -- We've known for a long time that "full of alcohol hurts", but a recent study provides new evidence of the dangers of long-term drinking.
deep in the brain, an area of the retinal amygdala plays a crucial role in showing emotions, behaviors, and motivations.
, the region is also affected by long-term drinking.
a recent study, Roberto and her team from the Scripps Institute first discovered the anti-inflammatory mechanisms of the amygdala and its effects on alcohol addiction.
the study was published in the journal Neurobiological Advances.
(Photo: www.pixabay.com) alcohol triggers a neuroimmune response in the brain, leading to alcohol use disorders (AUD) and continuity.
When inflammatory molecules begin to activate and drive neuroimmune responses, anti-inflammatory media provide an important alternative, however, our current understanding of the role of anti-inflammatory signals in key brain regions associated with pathological alcohol dependence behavior is limited, which prevents us from finding a cure for the symptoms in the short term.
study, the authors hypothesically assume that chronic alcohol intake impairs anti-inflammatory signals in the amygdala center.
because the amygdala is a brain region associated with worry and addiction, a permanent state of twisting drives abnormal activity in neurons and eventually leads to pathological outcomes.
Roberto specializes in an immunoprotein called lecierle interletin 10 or IL-10, which is common in the brain.
, IL-10 has powerful anti-inflammatory properties that ensure that the immune system is a threat to the disease in the brain, and IL-10 helps reduce disruption caused by injuries or diseases such as stroke or Alzheimer's disease.
it also seems to affect behaviors associated with long-term drinking.
study found that alcohol dependence alters the brain's overall immune response, leading to higher levels of small glial and Treg cells producing IL-10, while levels of IL-10 in local areas of the amygdala drop and do not signal neurons correctly, leading to increased alcohol intake in mice.
by expressing IL-10 over the amygdala region, the authors found that the mice's worried behavior decreased significantly and abnormal drinking behavior was suppressed, indicating its role in regulating amygdala-mediated behavior.
the mechanism, the IL-10 expressed by the amygdala directly regulates the GABA transmission at the front end of the synapse through the PI3K and p38 MAPK signals, and indirectly regulates the GABA transmission through changes in the self-dispensing power.
of the IR-10 signal began to gradually adapt, leading to a decrease in THE-10-induced GABA pass.
.
, the overexploitation of amygdala IL-10 eliminated alcohol dependence symptoms in mice, highlighting the shortcomings of amygdala IL-10 signaling in regulating neuron activity and underlying worrying behavior, as well as abnormally excessive drinking, and providing new options for the treatment and intervention of chronic drinking.
we have shown that the brain's inflammatory immune response plays a significant role in the development and maintenance of alcohol use disorders," said Roberto, a director of the Study Group.
but perhaps more importantly, we provide a new framework for therapeutic interventions that point to anti-inflammatory mechanisms.
" chronic drinking symptoms affect about 15 million people in the United States, with few effective treatments.
studying changes in brain cells after chronic drinking, Roberto's lab has found many new treatments for potential alcohol addicts.
future studies will be based on these findings to accurately identify how and when IL-10 sends signals to the amygdala and other neurons in the added brain circuit to change people's behavior toward alcohol.
() Source: Chronic alcohol use reshapes the brain's immune landscape, driving anxiety and addiction Original source: Reesha R. Patel et al, IL-10 normalizes aberrant amygdala GABA transmission and reverses anxiety-like-like and dependence-induced to the development of alcohol of 2020. DOI: 10.1016/j.pneurobio.2020.101952