Protein Information

ID 77
Name brains
Synonyms BPG dependent PGAM 1; Brain; CDABP0006; PGAM 1; PGAM B; PGAM1; PGAM1 protein; PGAMA…

Compound Information

ID 1708
Name ACC
CAS 1-aminocyclopropanecarboxylic acid

Reference

PubMed Abstract RScore(About this table)
17624993 Akine Y, Kato M, Muramatsu T, Umeda S, Mimura M, Asai Y, Tanada S, Obata T, Ikehira H, Kashima H, Suhara T: Altered brain activation by a false recognition task in young abstinent patients with alcohol dependence. Alcohol Clin Exp Res. 2007 Sep;31(9):1589-97. Epub 2007 Jul 11.
BACKGROUND: Heavy alcohol intake induces both structural and functional changes in the central nervous system. Recent research developments converged on the idea that even in patients with alcohol dependence without apparent structural brain changes, some cognitive impairment exists, and associated functional change could be visualized by neuroimaging techniques. However, these data were from old (more than 50 years) patients using working memory and response inhibition tasks. Whether young abstinent patients show aberrant signs of brain activation is a matter of interest, specifically by the long-term memory retrieval task. METHODS: Subjects were 9 young patients with alcohol dependence with long-term abstinent (8 males and 1 female) and age- and education-matched 9 healthy controls (7 males and 2 females). We used a modified false recognition task in a functional MRI study. RESULTS: The young patients with alcohol dependence showed reduced activation in the right dorsolateral prefrontal cortex, anterior cingulate cortex (ACC), left pulvinar in the thalamus, and in the right ventral striatum, although behavioral performances and regional patterns of brain activation were similar between patients and controls. CONCLUSIONS: Long-term memory retrieval induced altered activations in prefrontal lobes, ACC, thalamus, and ventral striatum in young patients with alcohol dependence. These findings were correspondent to deficits of goal directed behavior, monitoring the erroneous responses, memory function, and drug-seeking behavior. Furthermore, these reduced activations can be considered as latent "lesions," suggesting subclinical pathology in alcoholic brains.
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