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Titolo:
ARE MAO-A DEFICIENCY STATES IN THE GENERAL-POPULATION AND IN PUTATIVEHIGH-RISK POPULATIONS HIGHLY UNCOMMON
Autore:
MURPHY DL; SIMS K; EISENHOFER G; GREENBERG BD; GEORGE T; BERLIN F; ZAMETKIN A; ERNST M; BREAKEFIELD XO;
Indirizzi:
NIMH,CLIN SCI LAB,NIH,CTR CLIN,10-3D41,10 CTR DR MSC 1264 BETHESDA MD20892 NIMH,CHILD PSYCHIAT BRANCH,NIH BETHESDA MD 20892 MASSACHUSETTS GEN HOSP,MOL NEUROGENET LAB BOSTON MA 02114 NINCDS,CLIN NEUROSCI BRANCH,NIH BETHESDA MD 20892 NIAAA,CLIN STUDIES LAB,NIH BETHESDA MD 20892 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT BALTIMORE MD 21205
Titolo Testata:
Journal of neural transmission. Supplementum
fascicolo: 52, , anno: 1998,
pagine: 29 - 38
SICI:
0303-6995(1998):52<29:AMDSIT>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET MONOAMINE-OXIDASE; NORRIE DISEASE PATIENTS; CEREBROSPINAL-FLUID; B-GENES; PLASMA; METABOLISM; AMINE; NOREPINEPHRINE; INHIBITORS; DELETION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
D.L. Murphy et al., "ARE MAO-A DEFICIENCY STATES IN THE GENERAL-POPULATION AND IN PUTATIVEHIGH-RISK POPULATIONS HIGHLY UNCOMMON", Journal of neural transmission. Supplementum, (52), 1998, pp. 29-38

Abstract

Lack of monoamine oxidase A (MAO-A) due to either Xp chromosomal deletions or alterations in the coding sequence of the gene for this enzyme are associated with marked changes in monoamine metabolism and appear to be associated with variable cognitive deficits and behavioral changes in humans and in transgenic mice. In mice, some of the most marked behavioral changes are ameliorated by pharmacologically-induced reductions in serotonin synthesis during early development, raising the question of possible therapeutic interventions in humans with MAO deficiency states. At the present time, only one multi-generational family and a few other individuals with marked MAO-A deficiency states have been identified and studied in detail. Although MAO deficiency states associated with Xp chromosomal deletions were identified by distinct symptoms (including blindness in infancy) produced by the contiguous Norrie disease gene, the primarily behavioral phenotype of individuals with the MAO mutation is less obvious. This paper reports a sequential research design and preliminary results from screening several hundred volunteers in the general population and from putative high-risk groupsfor possible MAO deficiency states. These preliminary results suggestthat marked MAO deficiency states are very rare.

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Documento generato il 27/11/20 alle ore 23:58:07