Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic.
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Cognitive impairment is common following traumatic brain injury (TBI), and neuroinflammatory mechanisms may predispose to the development of neurodegenerative disease. Apolipoprotein E (apoE) polymorphisms modify neuroinflammatory responses, and influence both outcome from acute brain injury and the risk of developing neurodegenerative disease. We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele. The administration of an apoE-mimetic peptide markedly reduced the development of neurodegenerative pathology in mice homozygous for apoE3 as well as apoE3/E4 heterozygotes. These results demonstrate that TBI accelerates the cardinal neuropathological features of neurodegenerative disease, and establishes the potential for apoE mimetic therapies in reducing pathology associated with neurodegeneration.
Enzyme-Linked Immunosorbent Assay
Platelet-Derived Growth Factor
Tumor Necrosis Factor-alpha
Published Version (Please cite this version)10.1089/neu.2010.1396
Publication InfoLaskowitz, Daniel T; Song, Pingping; Wang, Haichen; Mace, Brian; Sullivan, Patrick M; Vitek, Michael P; & Dawson, Hana N (2010). Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic. J Neurotrauma, 27(11). pp. 1983-1995. 10.1089/neu.2010.1396. Retrieved from https://hdl.handle.net/10161/3293.
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Adjunct Assistant Professor in the Department of Neurology
Our laboratory studies the role of tau protein in neurodegeneration. Aggregated tau protein is a hallmark feature of a group of neurodegenerative dementias called tauopathies. This group of diseases accounts for a large majority of all dementias and includes Alzheimer's disease, Pick's disease and frontotemporal dementia to name a few. To model tauopathies, we overexpressed normal and mutated human tau protein or no tau protein in the central nervous system of transgenic mice. Several of t
Professor of Neurology
Our laboratory uses molecular biology, cell culture, and animal modeling techniques to examine the CNS response to acute injury. In particular, our laboratory examines the role of microglial activation and the endogenous CNS inflammatory response in exacerbating secondary injury following acute brain insult. Much of the in vitro work in this laboratory is dedicated to elucidating cellular responses to injury with the ultimate goal of exploring new therapeutic interventions in the clinical settin
Associate Professor of Medicine
The primary focus of my lab is to investigate the relationship between APOE genotype and late onset Alzheimer’s disease (AD). The single most common and influential gene in AD is the APOE gene. The APOE gene is polymorphic; encoding three different alleles designated APOE2, E3 or E4. APOE4 carriers have the highest risk for AD while APOE3 carriers have an essentially neutral risk and APOE2 carriers may be p
Adjunct Associate Professor in Neurology
The overall interest of my laboratory is to identify the underlying causes of neurodegenerative diseases such as Alzheimer's disease. Once causes or experimental endpoints are determined, then strategies to find chemicals which can ameliorate pathophysiological events can be devised. In general, we are working to create transgenic animals and validate them as models of human disease. Our specific approach has been to study the function of apolipoprotein-E (apoE) which
Assistant Professor of Neurology
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