Ivana Delalle, MD. PhD

JAD profile

Affiliation(s): 

Boston University School of Medicine; Boston Medical Center; Brigham and Women's Hospital

Areas of Interest: 

Alzheimer's disease; neurodegeneration; biomarkers

Biography & Research: 

I am clinician scientist presently focusing on: 1)Protein Expression of Alzheimer’s disease Risk Genetic Loci in Human Hippocampus. Genome-wide association studies (GWAS) have established BIN1 as the most important AD susceptibility locus after APOE. Genome-wide association studies established BIN1 as the most significant late-onset Alzheimer’s disease (AD) susceptibility locus after APOE. We found BIN1 protein expression in white matter, oligodendrocytes, astrocytes, and in neuropil where BIN1 signal decorated axonal neurofilaments. In CA1 and in prefrontal cortex of AD patients, however, BIN1-immunoreactive neuropil area significantly decreased while the percentage of BIN1-immunoreactive neuronal somata significantly increased among pyramidal neurons independent of tau pathology. The number of BIN1-immunoreactive CA1 neurons correlated positively with hippocampal CERAD neuritic plaque score. In addition, we recorded the absence of BIN1 neuropil signal at neuritic plaque sites. Alterations in CA1 BIN1 immunoreactivity patterns in the progressive stages of AD pathology were consistently present in the examined neocortical areas as well. Our data provide novel insight into the relationship between BIN1 protein expression and the progression of AD- associated pathology and its diagnostic hallmarks (Adams SL et al., JNEN 2016). 2) Epigenetic regulation in brain disorders. we have recently shown that: a) major cell categories in anterior cingulate cortex of BD patients differ in specific microRNA (miR) expression (PMID: 23382797), and b) extracellular vesicles extracted from prefrontal cortex harbor differential miR expression in patients diagnosed with either BD or SZ (PMID: 28190298). With Dr. Fischer at German Center for Degenerative Diseases at Goettingen University, we discovered a novel target to treat dementia (PMID: 24075854). In collaboration with the Tsai laboratory at Picower Institute for Learning and Memory at MIT, we showed that the expression of histone deacetylase 2, which reduces histone acetylation and thus expression of genes important for learning and memory, increases during the progression of Alzheimer’s disease (PMID: 22388814). My Bibliography (public) http://www.ncbi.nlm.nih.gov/sites/myncbi/1l3xh9ikpycQu/bibliography/47824278/public/?sort=date&direction=ascending. Other citations (public) http://www.ncbi.nlm.nih.gov/sites/myncbi/1l3xh9ikpycQu/bibliography/47824279/public/?sort=date&direction=ascending.