Journal ArticleProg Neurobiol · September 2022 Lewy body disorders are characterized by oxidative damage to DNA and inclusions rich in aggregated forms of α-synuclein. Among other roles, apurinic/apyrimidinic endonuclease 1 (APE1) repairs oxidative DNA damage, and APE1 polymorphisms have been linked to ... Full textLink to itemCite
Journal ArticleFaseb Journal : Official Publication of the Federation of American Societies for Experimental Biology · May 1, 2022 Lewy body disorders are characterized by proteostatic and redox disequilibrium, leading to deposition of α-synuclein in hallmark inclusions and oxidative damage to DNA. One common pathway for repair of oxidative DNA damage is base excision repair (BER), wh ... Full textCite
Journal ArticleBiosens Bioelectron · January 15, 2022 Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative brain disorder that affects tens of millions of older adults worldwide and has significant economic and societal impacts. Despite its prevalence and severity, early diagnosis of A ... Full textLink to itemCite
Journal ArticleJ Neurosci Res · January 2021 Parkinson's disease (PD) is the most common movement neurodegenerative disorder. Although our understanding of the underlying mechanisms of pathogenesis in PD has greatly expanded, this knowledge thus far has failed to translate into disease-modifying ther ... Full textLink to itemCite
Journal ArticleAm J Pathol · December 2020 Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of familial Parkinson disease. Although LRRK2-related Parkinson disease patients have a heightened risk of certain nonskin cancers, including breast cancer, it is unknown ... Full textLink to itemCite
Journal ArticleSci Rep · October 14, 2020 Leucine-rich repeat kinase 2 (LRRK2) is a promising therapeutic target for the treatment of Parkinson's disease (PD) and LRRK2 kinase inhibitors are currently being tested in early phase clinical trials. In order to ensure the highest chance of success, a ... Full textLink to itemCite
Journal ArticleNat Commun · November 19, 2018 While young muscle is capable of restoring the original architecture of damaged myofibers, aged muscle displays a markedly reduced regeneration. We show that expression of the "anti-aging" protein, α-Klotho, is up-regulated within young injured muscle as a ... Full textLink to itemCite
Journal ArticleJ Neurosci · August 22, 2018 Dysregulation of mitochondrial biogenesis is implicated in the pathogenesis of neurodegenerative diseases such as Parkinson's disease (PD). However, it is not clear how mitochondrial biogenesis is regulated in neurons, with their unique compartmentalized a ... Full textLink to itemCite
Journal ArticleSci Transl Med · July 25, 2018 Missense mutations in leucine-rich repeat kinase 2 (LRRK2) cause familial Parkinson's disease (PD). However, a potential role of wild-type LRRK2 in idiopathic PD (iPD) remains unclear. Here, we developed proximity ligation assays to assess Ser1292 phosphor ... Full textLink to itemCite
Journal ArticleCurr Protoc Toxicol · May 2018 Given the crucial role of DNA damage in human health and disease, it is important to be able to accurately measure both mitochondrial and nuclear DNA damage. This article describes a method based on a long-amplicon quantitative PCR-based assay that does no ... Full textLink to itemCite
Journal ArticleCurrent Opinion in Toxicology · February 1, 2018 DNA damage is any modification to the structure of DNA that alters its coding properties and/or interferes with cell processes. One major consequence of oxidative stress is DNA damage, which include base modifications, abasic sites, and strand breaks. A wi ... Full textCite
Journal ArticleJ Biol Chem · January 26, 2018 It has been long assumed that post-mitotic neurons only utilize the error-prone non-homologous end-joining pathway to repair double-strand breaks (DSBs) associated with oxidative damage to DNA, given the inability of non-replicating neuronal DNA to utilize ... Full textLink to itemCite
Journal ArticleNeurobiol Dis · January 2018 Parkinson's disease (PD) is a complex, chronic and progressive neurodegenerative disease. While the etiology of PD is likely multifactorial, the protein α-synuclein is a central component to the pathogenesis of the disease. However, the mechanism by which ... Full textLink to itemCite
Journal ArticleHum Mol Genet · November 15, 2017 Mutations in leucine-rich repeat kinase 2 (LRRK2) are associated with increased risk for developing Parkinson's disease (PD). Previously, we found that LRRK2 G2019S mutation carriers have increased mitochondrial DNA (mtDNA) damage and after zinc finger nuc ... Full textLink to itemCite
Journal ArticleCell Mol Life Sci · August 2017 Intracellular accumulation of α-synuclein (α-syn) are hallmarks of synucleinopathies, including Parkinson's disease (PD). Exogenous addition of preformed α-syn fibrils (PFFs) into primary hippocampal neurons induced α-syn aggregation and accumulation. Like ... Full textLink to itemCite
Journal ArticleToxicol Sci · July 1, 2017 Exposure to certain pesticides induces oxidative stress and increases Parkinson's disease (PD) risk. Mitochondrial DNA (mtDNA) damage is found in dopaminergic neurons in idiopathic PD and following pesticide exposure in experimental models thereof. Base ex ... Full textLink to itemCite
Journal ArticleMol Cell Neurosci · July 2017 The presence of Lewy bodies, mainly consisting of aggregated α-synuclein, is a pathological hallmark of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). The α-synuclein inclusions are predominantly found in neurons, but also appear frequently ... Full textLink to itemCite
Chapter · October 13, 2016 Featured Publication This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. ...