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Allan L. Reiss

Researcher at Stanford University

Publications -  553
Citations -  64704

Allan L. Reiss is an academic researcher from Stanford University. The author has contributed to research in topics: Fragile X syndrome & Autism. The author has an hindex of 118, co-authored 529 publications receiving 59363 citations. Previous affiliations of Allan L. Reiss include Johns Hopkins University School of Medicine & University of California, San Diego.

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Brain imaging in neurogenetic conditions: realizing the potential of behavioral neurogenetics research.

TL;DR: This paper reviews five genetic conditions that commonly give rise to identifiable neurodevelopmental and neuropsychiatric disability in children: fragile X syndrome, velo-cardio-facial syndrome, Williams syndrome, Turner syndrome, and Klinefelter syndrome.
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Developmental changes in multivariate neuroanatomical patterns that predict risk for psychosis in 22q11.2 deletion syndrome

TL;DR: Novel evidence of morphometric spatial patterns predicting the development of psychotic symptoms in 22q11.2DS is shown, and the use of neuroimaging using MVPA may hold promise to predict outcome in a variety of neuropsychiatric disorders.
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A prospective test of the association between hyperarousal and emotional numbing in youth with a history of traumatic stress.

TL;DR: Investigated the hypothesis that emotional numbing may develop as a result of hyperarousal using a prospective design and indicated that hyperarrousal symptoms were concurrently positively correlated with emotional numting at both time points.
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Reduced size of the amygdala in individuals with 47,XXY and 47,XXX karyotypes.

TL;DR: The alteration in amygdala volumes in individuals with a supernumerary X chromosome may provide a neuroanatomic basis for the findings of variations in volumes of mesial temporal lobe structures in men and women with SCA.
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Hippocampal volume, PTSD, and alcoholism in combat veterans

TL;DR: The failure to observe a strong association between PTSD and hippocampal volume in nonalcoholic subjects was not ascribable to younger age, reduced PTSD chronicity, or lower PTSD symptom severity, and the possibility that smaller hippocampusal volume is limited to groups in which PTSD is compounded by comorbid alcoholism is not necessarily incompatible with results suggesting a smaller hippocampus is predispositional to PTSD.