Abstract
Alzheimer’s disease (AD) is a syndrome caused by a few uncommon mutations that lead to early-onset disease, occurs in adults with Down’s syndrome, but is by far most commonly seen as a late-onset disease with multiple risk factors but no causative factors yet identified. Emerging data suggests a chronic disease model for AD with latency, prodrome, and dementia stages together lasting decades. Free radical damage to lipids in brain is one pathogenic process of AD that may be quantified with F2-isoprostanes (IsoPs). Whereas brain and cerebrospinal fluid (CSF) F2-IsoPs are reproducibly elevated in AD patients at both dementia and prodromal stages of disease, plasma and urine F2-IsoPs are not reproducibly increased in AD patients. CSF F2-IsoPs may be used to assist in diagnosis and aid in objective assessment of disease progression and response to therapeutics in patients with AD.
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This work was supported by the Nancy and Buster Alvord Endowment and grants from the NIH (AG05136, AG23801, and AG24011).
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Montine, T.J., Quinn, J., Kaye, J. et al. F2-Isoprostanes as Biomarkers of Late-onset Alzheimer’s Disease. J Mol Neurosci 33, 114–119 (2007). https://doi.org/10.1007/s12031-007-0044-1
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DOI: https://doi.org/10.1007/s12031-007-0044-1