We computationally matched the juvenile plasticity signature to 436 disease signatures derived from public microarray data. This systematic method applies a rank-based molecular matching algorithm to determine the molecular concordance between the plasticity signature and a given disease signature, where high scores indicate that plasticity genes are significantly dysregulated by the disease and low scores indicate that the disease has no impact on plasticity genes. Highly ranked diseases included not only brain disorders known to disrupt plasticity such as Huntington’s disease, but also non-neurologic disorders (e.g., bacterial infections, inflammatory bowel disease, metabolic diseases), suggesting that a broad range of disease states may impact molecular pathways involved in plasticity. ALS, Amyotrophic lateral sclerosis; AML, acute myeloid leukemia; APECED, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy; CBCL, cutaneous B-cell lymphoma; CFS, chronic fatigue syndrome; CML, chronic myeloid leukemia; COPD, chronic obstructive pulmonary disease; DMD, Duchenne muscular dystrophy; FDIU, fetal death in utero; FDR, false discovery rate; GERD, gastroesophageal reflux disease; HIV, human immunodeficiency virus; IBD, inflammatory bowel disease; IBS, irritable bowel syndrome; IUGR, intrauterine growth retardation; JRA, juvenile rheumatoid arthritis; LGLL, large granular lymphocytic leukemia; MCTD, mixed connective tissue disease; MDS, myelodysplastic syndrome; MGUS, Monoclonal gammopathy of undetermined significance; MMHCC, Mouse Models of Human Cancers Consortium; MODY, maturity onset diabetes in youth type 1; MS, multiple sclerosis; PBL, peripheral blood lymphocyte; PTSD, post-traumatic stress disorder; RA, rheumatoid arthritis; SARS, severe acute respiratory syndrome; SCID, severe combined immunodeficiency.