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Transcriptional control of maladaptive and protective responses in alcoholics : a role of the NF-κB system

Yakovleva, Tatjana (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Molecular neuropsychopharmacology
Bazov, Igor (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Molecular neuropsychopharmacology
Watanabe, Hiroyuki (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Molecular neuropsychopharmacology
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Hauser, Kurt (författare)
Bakalkin, Georgy (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Molecular neuropsychopharmacology
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 (creator_code:org_t)
Elsevier BV, 2010
2010
Engelska.
Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 25:Suppl. 1, s. S29-S38
  • Forskningsöversikt (refereegranskat)
Abstract Ämnesord
Stäng  
  • Alcohol dependence and associated cognitive impairment appear to result from maladaptive neuroplasticity in response to chronic alcohol consumption, neuroinflammation and neurodegeneration. The inherent stability of behavioral alterations associated with the addicted state suggests that transcriptional and epigenetic mechanisms are operative. NF-κB transcription factors are regulators of synaptic plasticity and inflammation, and responsive to a variety of stimuli including alcohol. These factors are abundant in the brain where they have diverse functions that depend on the composition of the NF-κB complex and cellular context. In neuron cell bodies, NF-κB is constitutively active, and involved in neuronal injury and neuroprotection. However, at the synapse, NF-κB is present in a latent form and upon activation is transported to the cell nucleus. In glia, NF-κB is inducible and regulates inflammatory processes that exacerbate alcohol-induced neurodegeneration. Animal studies demonstrate that acute alcohol exposure transiently activates NF-κB, which induces neuroinflammatory responses and neurodegeneration. Postmortem studies of brains of human alcoholics suggest that repeated cycles of alcohol consumption and withdrawal cause adaptive changes in the NF-κB system that may permit the system to better tolerate excessive stimulation. This type of tolerance, ensuring a low degree of responsiveness to applied stimuli, apparently differs from that in the immune system, and may represent a compensatory response that protects brain cells against alcohol neurotoxicity. This view is supported by findings showing preferential downregulation of pro-apoptotic gene expression in the affected brain areas in human alcoholics. Although further verification is needed, we speculate that NF-κB-driven neuroinflammation and disruption to neuroplasticity play a significant role in regulating alcohol dependence and cognitive impairment.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Farmaceutiska vetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Pharmaceutical Sciences (hsv//eng)

Nyckelord

alcoholism
dependence
addiction
neuroinflammation
neuroplasticity
gene transcription
transcription factors
NF-κB
p50
human brain
PHARMACY
FARMACI

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