Genomes and Genes
Affiliation: University of California
- Perinatal programming of neurodevelopment: epigenetic mechanisms and the prenatal shaping of the brainPaula A Desplats
Department of Neurosciences, University of California San Diego, La Jolla, CA, USA
Adv Neurobiol 10:335-61. 2015..As novel techniques emerge and as genome-wide profiling of disease-associated methylomes is achieved, epigenetic marks open a new source for biomarker discovery. ..
- Combined exposure to Maneb and Paraquat alters transcriptional regulation of neurogenesis-related genes in mice models of Parkinson's diseasePaula Desplats
Department of Neuroscience, University of California San Diego, 9500 Gilman Dr, MTF 344, La Jolla, CA 92093 0624, USA
Mol Neurodegener 7:49. 2012..While PD is characterized by neuronal loss in the substantia nigra, we previously showed that accumulation of α-synuclein in the limbic system contributes to neurodegeneration by interfering with adult neurogenesis...
- α-Synuclein induces alterations in adult neurogenesis in Parkinson disease models via p53-mediated repression of Notch1Paula Desplats
Department of Neurosciences, School of Medicine, University of California San Diego, La Jolla, California 92093, USA
J Biol Chem 287:31691-702. 2012..This study provides a molecular basis for α-synuclein-mediated disruption of adult neurogenesis in Parkinson disease...
- Alpha-synuclein sequesters Dnmt1 from the nucleus: a novel mechanism for epigenetic alterations in Lewy body diseasesPaula Desplats
Department of Neurosciences, School of Medicine, University of California at San Diego, La Jolla, California 92093, USA
J Biol Chem 286:9031-7. 2011..Our results underscore a novel mechanism for epigenetic dysregulation in Lewy body diseases, which might underlie the decrease in DNA methylation reported for PD and DLB...
- Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synucleinPaula Desplats
Department of Neurosciences and Pathology, School of Medicine, University of California at San Diego, La Jolla, CA 92093, USA
Proc Natl Acad Sci U S A 106:13010-5. 2009..These findings demonstrate the cell-to-cell transmission of alpha-synuclein aggregates and provide critical insights into the mechanism of pathological progression in PD and other proteinopathies...
- Alpha-synuclein alters Notch-1 expression and neurogenesis in mouse embryonic stem cells and in the hippocampus of transgenic miceLeslie Crews
Departments of Neurosciences, University of California, San Diego, La Jolla, California 92093 0624, USA
J Neurosci 28:4250-60. 2008..Together, these results suggest that accumulation of alpha-syn might impair survival of NPCs by interfering with the Notch signaling pathway. Similar mechanisms could be at play in PD and Lewy body disease...
- Mechanisms of hybrid oligomer formation in the pathogenesis of combined Alzheimer's and Parkinson's diseasesIgor F Tsigelny
Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, California, United States of America
PLoS ONE 3:e3135. 2008..However the molecular characteristics and consequences of these interactions are not completely clear...
- Selective molecular alterations in the autophagy pathway in patients with Lewy body disease and in models of alpha-synucleinopathyLeslie Crews
Department of Pathology, University of California San Diego, La Jolla, California, United States of America
PLoS ONE 5:e9313. 2010..For this reason, we sought to examine the expression levels of members of the autophagy pathway in brains of patients with DLB and Alzheimer's Disease (AD) and in alpha-synuclein transgenic mice...
- Hippocampal neuronal cells that accumulate α-synuclein fragments are more vulnerable to Aβ oligomer toxicity via mGluR5--implications for dementia with Lewy bodiesCassia R Overk
Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
Mol Neurodegener 9:18. 2014..In this context, the main objective of the present study was to investigate the role of mGluR5 as a mediator of the neurotoxic effects of α-syn and Aβ in the hippocampus...
- In vivo alterations in calcium buffering capacity in transgenic mouse model of synucleinopathyLidia Reznichenko
Department of Neurosciences, University of California, San Diego, La Jolla, California 92093, USA
J Neurosci 32:9992-8. 2012....
- Increased CDK5 expression in HIV encephalitis contributes to neurodegeneration via tau phosphorylation and is reversed with RoscovitineChristina Patrick
Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093 0624, USA
Am J Pathol 178:1646-61. 2011..These findings indicate that abnormal CDK5 activation contributes to the neurodegenerative process in HIVE via abnormal tau phosphorylation; thus, reducing CDK5 might ameliorate the cognitive impairments associated with HIVE...
- Alterations in mGluR5 expression and signaling in Lewy body disease and in transgenic models of alpha-synucleinopathy--implications for excitotoxicityDiana L Price
Department of Neurosciences, University of California San Diego, La Jolla, California, United States of America
PLoS ONE 5:e14020. 2010..These results highlight the therapeutic importance of mGluR5 antagonists in alpha-synucleinopathies...
- Epigenetic alterations in the brain associated with HIV-1 infection and methamphetamine dependencePaula Desplats
Department of Neuroscience, University of California San Diego, La Jolla, California, United States of America
PLoS ONE 9:e102555. 2014..Importantly, we identified new epigenetic targets that might aid in understanding the aggravated neurodegenerative, cognitive, motor and behavioral symptoms observed in persons living with HIV and addictions. ..
- Antibody-aided clearance of extracellular α-synuclein prevents cell-to-cell aggregate transmissionEun Jin Bae
Department of Biomedical Science and Technology, Konkuk University, Seoul 143 701, Korea
J Neurosci 32:13454-69. 2012..These findings provide an underlying mechanistic basis for immunotherapy for PD/DLB and suggest extracellular forms of α-synuclein as potential therapeutic targets...
- TOM40 mediates mitochondrial dysfunction induced by α-synuclein accumulation in Parkinson's diseaseAndreas Bender
Department of Neurology with Friedrich Baur Institute, University of Munich, Munich, Germany
PLoS ONE 8:e62277. 2013..Our results suggest that alterations in the mitochondrial protein transport machinery might contribute to mitochondrial impairment in α-Synucleinopathies...
- Molecular and pathologic insights from latent HIV-1 infection in the human brainPaula Desplats
Department of Neurosciences, University of California San Diego, La Jolla, USA
Neurology 80:1415-23. 2013..We aimed to investigate whether HIV latency in the CNS might have adverse molecular, pathologic, and clinical consequences...
- Structural diversity of Alzheimer's disease amyloid-β dimers and their role in oligomerization and fibril formationIgor F Tsigelny
San Diego Supercomputer Center, University of California, San Diego, La Jolla, CA, USA Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA
J Alzheimers Dis 39:583-600. 2014..Our studies suggest a greater diversity of Aβ dimers. Understanding the structure of Aβ dimers might be important for the rationale design of small molecules that block formation of toxic oligomers. ..