The Science of Alzheimer’s Disease

The Department of Psychiatry leads the field of neurodegenerative disorders by characterization of the human gene promoter regions that are viable drug targets for Alzheimer’s disease. IU School of Medicine researchers discovered that the Alzheimer’s-associated amyloid-beta peptide is a gene transcription factor by discovering its DNA target motif and demonstrating target-associated chromosomal co-location in vivo, functional activity and effects of altering the target motif.

IU School of Medicine experts found micro-ribonucleic acid (RNA) operating on Alzheimer’s-associated microRNAs and that levels of specific miRNA species could be novel markers for Alzheimer’s disease risk. Department of Psychiatry experts are investigating co-regulation of Alzheimer’s disease and traumatic brain injury (TBI) associated protein levels by miRNA species.

The latent early-life associated regulation (LEARn) model suggests that early-life exposures may be latently stored in the epigenome until sufficient hits accumulate to produce Alzheimer’s disease or other late-life disorders. To unite the influences of environment, epigenomics, genomics and family history, the Longitudinal Everything-Wide Association Study (LEWAS) model traces development of a disorder as a process.

Current treatments for Alzheimer’s disease grant temporary relief but show little sign of slowing the course of the disease. The Department of Psychiatry uses regulatory-based work as a rational, molecular treatment strategy for Alzheimer’s disease. The IU School of Medicine is working toward identifying molecular pathways contributing to cellular degeneration well ahead of current genomic customization.

Alzheimer’s disease and autism could potentially have fundamental molecular oppositions and fundamental molecular links. Department of Psychiatry experts compare the amyloid-beta peptide processing pathways associated with Alzheimer’s disease with those of autism.