Age by Disease molecular interactions.


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.



– 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.