Age by Disease molecular interactions.

Overview:

We have shown that aging represents the largest source of biological variability in transcriptome in the human postmortem brain, and have characterized its nature, extent and gene/ pathway specificities. Findings from our group demonstrate that these age-related changes include neuropsychiatric and neurodegenerative disease pathways and may promote disease. These experimental findings have been conceptualized in a novel age-by-disease interaction hypothesis, which we are now testing at the genetic levels, using a combined human postmortem brain and epidemiological cohort research approach.

 

Publications:

– Pabba M, Scifo E, Kapadia F, Nikolova YS, Ma T, Mechawar N, Tseng GC, Sibille E. Resilient protein co-expression network in male orbitofrontal cortex layer 2/3 during human aging. Neurobiol Aging. 2017 Oct;58:180-190. PubMed PMID: 28750307; PubMed Central PMCID: PMC5581682.

– Ding Y, Chang LC, Wang X, Guilloux JP, Parrish J, Oh H, French BJ, Lewis DA, Tseng GC, Sibille E. Molecular and Genetic Characterization of Depression: Overlap with other Psychiatric Disorders and Aging. Mol Neuropsychiatry. 2015 May;1(1):1-12. PubMed PMID: 26213687; PubMed Central PMCID: PMC4512183.

– Douillard-Guilloux G, Guilloux JP, Lewis DA, Sibille E. Anticipated brain molecular aging in major depression. Am J Geriatr Psychiatry. 2013 May;21(5):450-60. PubMed PMID: 23570888; PubMed Central PMCID: PMC3615087.

– Sibille E. Molecular aging of the brain, neuroplasticity, and vulnerability to depression and other brain-related disorders. Dialogues Clin Neurosci. 2013 Mar;15(1):53-65. PubMed PMID: 23576889; PubMed Central PMCID: PMC3622469.