In general, we are exploring what goes wrong in the brains of patients with neurodegenerative diseases, especially Alzheimer’s disease (AD) and Frontal Temporal lobe Degeneration linked to tauopathy (FTD-tau) with the overall aim of identifying therapeutic approaches that may be beneficial for the treatment, or prevention of these diseases. Given our broad interest in neurodegenerative disease etiology and the insights to be gained by studying different diseases my lab has created various mouse models for the study of AD (amyloid accumulation), tauopathies and synucleinopathies. These models have facilitated the study of many aspects of pathogenesis from how the disease propagates through the brain, to imaging studies allowing the examination of structural and functional changes in the brain in living animals, to the identification of relevant druggable pathways and the testing of drugs. Our current interests are fourfold: the propagation of disease through the brain; the impact of ApoE4 on disease risk; the impact and restoration of functional clearance mechanisms; and the basis and manipulation of memory deficits using optogenetic and brain stimulation techniques There are currently four projects underway in the lab. One recent undertaking is to identify new pathways impacted by ApoE genotype that might explain why inheritance of ApoE4 allele increases risk for AD using a multi-omics approach (transcriptomics, lipidomics and metabolomics) on the same, pathology free human or ApoE targeted mouse brain tissue. As the brains of AD patients often show multiple pathologies and accumulate several different types of potentially neurotoxic misfolded proteins including Abeta, tau, synuclein and TDP-43, we are currently focused on understanding the role of misfolded protein clearance pathways (mainly autophagy and UPS clearance) in disease etiology. ![]() Neurobiology Of Disease In Children![]() ![]() Neurobiology Of Disease Impact FactorIn addition, as clinical trials using Abeta immunotherapy have suggested that reducing Abeta/amyloid in mild-moderate AD patients has no effect on their tauopathy, which continues to propagate, it would seem that drugs aimed at clearing all misfolded protein types from the brain would be beneficial. It also seems likely that we will need to intervene very early in the disease, perhaps prophylactically, and at this time, very little is known of disease initiation and the earliest stages of propagation as most of the animal models that we, and others have generated do not accurately model the spatial and temporal sequence of the disease. Our more recent work modeling AD tauopathy using wild-type genomic (BAC derived) tau constructs has aimed to more faithfully replicate spatio-temporal aspects of tauopathy in AD, and current work aims to explore cellular and circuit vulnerability that defines a particular neurodegenerative disease. We have recently created a line of mice that models the earliest Braak stages of AD, when tauopathy is restricted to the entorhinal cortex (EC) and hippocampus. Download Free PDF Viewer Nokia N70 Apps to your Nokia N70. [NEW UPDATE] Adobe Reader for Symbian OS software lets you to view Adobe PDF. Download adobe pdf reader for nokia n70 download. PDF Reader 3.3. PDF Reader is a free and small program to view, modify and print pdf files. Download now. Size: 3.69MB License: Freeware Price: Free By:. Adobe Reader for Symbian - Download Adobe PDF files to your Symbian device a number of ways - from the Internet, as e-mail attachments, or from your desktop. Quicker launch times mean you can open PDF files faster than ever. Use Adobe Reader on your Nokia Smartphone to easily.
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