Abstract:
:Alcohol exposure during fetal and early postnatal development can lead to an increased incidence of later life adult-onset diseases. Examples include central nervous system dysfunction, depression, anxiety, hyperactivity, and an inability to deal with stressful situations, increased infection and cancer. Direct effects of alcohol leading to developmental abnormalities often involve epigenetic modifications of genes that regulate cellular functions. Epigenetic marks carried over from the parents are known to undergo molecular programming events that happen early in embryonic development by a wave of DNA demethylation, which leaves the embryo with a fresh genomic composition. The proopiomelanocortin (Pomc) gene controls neuroendocrine-immune functions and is imprinted by fetal alcohol exposure. Recently, this gene has been shown to be hypermethylated through three generations. Additionally, the alcohol epigenetic marks on the Pomc gene are maintained in the male but not in the female germline during this transgenerational transmission. These data suggest that the male-specific chromosome might be involved in transmitting alcohol epigenetic marks through multiple generations.
journal_name
Addict Bioljournal_title
Addiction biologyauthors
Sarkar DKdoi
10.1111/adb.12186subject
Has Abstractpub_date
2016-01-01 00:00:00pages
23-34issue
1eissn
1355-6215issn
1369-1600journal_volume
21pub_type
杂志文章,评审abstract::Activation of brain microglial cells, microgliosis, has been linked to methamphetamine (MA)-seeking behavior, suggesting that microglia could be a new therapeutic target for MA use disorder. Animal data show marked brain microglial activation following acute high-dose MA, but microglial status in human MA users is unc...
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Addiction biology
pub_type: 杂志文章
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journal_title:Addiction biology
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