scispace - formally typeset
J

Joel E. Kleinman

Researcher at Johns Hopkins University

Publications -  465
Citations -  33042

Joel E. Kleinman is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Prefrontal cortex & Dorsolateral prefrontal cortex. The author has an hindex of 92, co-authored 436 publications receiving 29593 citations. Previous affiliations of Joel E. Kleinman include United States Department of Health and Human Services & Johns Hopkins University School of Medicine.

Papers
More filters
Journal ArticleDOI

Spatio-temporal transcriptome of the human brain

TL;DR: The generation and analysis of exon-level transcriptome and associated genotyping data, representing males and females of different ethnicities, from multiple brain regions and neocortical areas of developing and adult post-mortem human brains, finds that 86 per cent of the genes analysed were expressed, and that 90 per cent were differentially regulated at the whole-transcript or exon level acrossbrain regions and/or time.
Journal ArticleDOI

Functional Analysis of Genetic Variation in Catechol-O-Methyltransferase (COMT): Effects on mRNA, Protein, and Enzyme Activity in Postmortem Human Brain

TL;DR: Val is a predominant factor that determines higher COMT activity in the prefrontal cortex, which presumably leads to lower synaptic dopamine levels and relatively deleterious prefrontal function.
Journal ArticleDOI

Temporal dynamics and genetic control of transcription in the human prefrontal cortex

TL;DR: The temporal dynamics and genetic control of transcription in human prefrontal cortex in an extensive series of post-mortem brains from fetal development through ageing is explored, finding a wave of gene expression changes occurring during fetal development which are reversed in early postnatal life.
Journal ArticleDOI

Integrative functional genomic analysis of human brain development and neuropsychiatric risks

TL;DR: The generation and analysis of a variety of genomic data modalities at the tissue and single-cell levels, including transcriptome, DNA methylation, and histone modifications across multiple brain regions ranging in age from embryonic development through adulthood, reveal insights into neurodevelopment and the genomic basis of neuropsychiatric risks.