Project description:While mouse models of ß-amyloidopathy recapitulate aspects of Alzheimer's disease pathology, including plaque formation and synapse loss, most progress at a speed such that outcomes are studied in the mature mouse, rather than the aged mouse. Here we investigated Aß-dependent changes to astrocytes in a knock-in model of ß-amyloidopathy (APP NL-F) that is known to progress more slowly.
Project description:Liquid chromatography mass spectrometry was used to study tumor matrisome from laser capture microdissected FFPE tissue sections of human neck and squamous cell carcinoma (HnSCC) xenograft grown in mouse.
Project description:Gene expression profiling of the epithelial and mesenchymal compartments of the developing mouse tooth using Laser Capture Microdissected (LCM) or enzymatic treatment with Dispase to isolate the dental epithelial and mesenchymal tissue, over a developmental period from E10.0-E14.5. The data is also accessible from http://compbio.med.harvard.edu/ToothCODE/
Project description:We performed gene expression profiling of laser capture microdissected normal non-neoplastic prostate (cystoprostatectomies) epithelial tissue and compared it to non-transformed and neoplastic low and high grade prostate epithelial tissue from radical prostatectomies, each with its immediately surrounding stroma.
Project description:The deposition of amyloid senile plaques (SPs) plays a central role in Alzheimer’s disease (AD), but the mechanisms by which SPs induce neural toxicity are disputed. Genetically engineered mouse models emphasizing SPs have had limited success in reproducing the neuropathology of AD, and have also failed to be good indicators of successful amyloid-targeting therapies. Therefore, it is fundamentally important to fully characterize and distinguish the pathological changes elicited by SPs in human and mouse brains. Using laser capture microdissection (LCM) combined with high-throughput mass spectrometry, we quantified ~5000 proteins with high confidence in SPs and non-plaque regions from APP/PS1 mouse model brain. We found more proteomic alteration in SPs than in non-plaque regions, and identified more than 200 mouse proteins that were significantly enriched in SPs. Together, our findings represent the most systematic analysis of the sub-proteome of SPs and provide a framework for future studies on plaque pathology and AD progression.
Project description:In this study, we combined cell-specific laser capture and RNA-seq analysis to investigate transcriptome changes in both amyloid-ß plaque-associated and plaque-distant microglia at different stages of the disease.
