Research Topics
Genomes and Genes | P Hemachandra ReddySummaryAffiliation: Oregon Health and Science University Country: USA Publications
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Publications
Is the mitochondrial outermembrane protein VDAC1 therapeutic target for Alzheimer's disease?P Hemachandra Reddy
Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA
Biochim Biophys Acta 1832:67-75. 2013..The purpose of this article is to review research that has investigated the relationship between VDAC1 and the regulation of MPT pores in AD progression...- Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer's disease: implications to mitochondria-targeted antioxidant therapeuticsP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1822:639-49. 2012..This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease... - Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1822:101-10. 2012..This article also discusses the therapeutic strategies that decrease mitochondrial fragmentation and neuronal damage in HD... 
Mapping cellular transcriptosomes in autopsied Alzheimer's disease subjects and relevant animal modelsP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Neurobiol Aging 27:1060-77. 2006..The major finding from these studies is that AD progression and pathogenesis involve multiple cellular pathways, which suggests that AD is a complex and heterogeneous disease...- Mitochondrial medicine for aging and neurodegenerative diseasesP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Neuromolecular Med 10:291-315. 2008.... - Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's diseaseP Hemachandra Reddy
Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, 97006, USA
Exp Neurol 218:286-92. 2009..This article also discusses the link between Abeta and impaired mitochondrial dynamics in AD... - Mitochondrial structural and functional dynamics in Huntington's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health and Science University, Beaverton, OR 97006, USA
Brain Res Rev 61:33-48. 2009..Further, this article outlines the current status of mitochondrial therapeutics with a special reference to Dimebon... - Granulocyte-macrophage colony-stimulating factor antibody suppresses microglial activity: implications for anti-inflammatory effects in Alzheimer's disease and multiple sclerosisP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon 97006, USA
J Neurochem 111:1514-28. 2009..The findings from this study may have implications for anti-inflammatory effects of Alzheimer's disease and experimental autoimmune encephalomyelitis mice (a multiple sclerosis mouse model)... - Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive declineP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Beaverton, OR, USA
J Alzheimers Dis 20:S499-512. 2010..This paper also briefly discusses potential mitochondrial therapeutics in the treatment of patients with AD... - Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Brain Res 1415:136-48. 2011..This article evaluates the role of tau in mitochondrial dysfunction and assesses how hyperphosphorylated tau impairs axonal transport of organelles in AD neurons... - Dynamin-related protein 1 and mitochondrial fragmentation in neurodegenerative diseasesP Hemachandra Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Brain Res Rev 67:103-18. 2011.... - Mitochondria as a therapeutic target for aging and neurodegenerative diseasesP H Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA
Curr Alzheimer Res 8:393-409. 2011..It also outlines mitochondria-targeted therapeutics in neurodegenerative diseases... - Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Trends Mol Med 14:45-53. 2008..Here, we describe recent studies regarding the roles of Abeta and mitochondrial function in AD progression and particularly in synaptic damage and cognitive decline... - Mitochondrial dysfunction in aging and Alzheimer's disease: strategies to protect neuronsP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006, USA
Antioxid Redox Signal 9:1647-58. 2007..This article discusses critical issues of mitochondria causing dysfunction in aging and AD and discusses the strategies to protect neurons caused by mitochondrial dysfunction... - Are mitochondria critical in the pathogenesis of Alzheimer's disease?P Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Brain Res Brain Res Rev 49:618-32. 2005..Findings from biochemical studies, in vitro studies, gene expression studies, and animal model studies of AD are reviewed, and the possible contribution of mitochondrial mutations to late-onset sporadic AD is discussed... - Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, OR 97006, USA
Hum Mol Genet 13:1225-40. 2004..These findings have important implications for understanding the mechanism of Abeta toxicity in AD and for developing therapeutic strategies for AD... - Differential loss of synaptic proteins in Alzheimer's disease: implications for synaptic dysfunctionP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 N W 185th Avenue, Beaverton, OR 97006, USA
J Alzheimers Dis 7:103-17; discussion 173-80. 2005..Our study suggests that postsynaptic proteins and presynaptic proteins are important for synaptic function and may be related to cognitive impairments in AD... - Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's diseaseUlziibat P Shirendeb
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Hum Mol Genet 21:406-20. 2012.... - Mitochondria-targeted antioxidants protect against amyloid-beta toxicity in Alzheimer's disease neuronsMaria Manczak
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR, USA
J Alzheimers Dis 20:S609-31. 2010..These findings suggest that MitoQ and SS31 prevent Abeta toxicity, which would warrant the study of MitoQ and SS31 as potential drugs to treat patients with AD... - Abnormal mitochondrial dynamics, mitochondrial loss and mutant huntingtin oligomers in Huntington's disease: implications for selective neuronal damageUlziibat Shirendeb
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Hum Mol Genet 20:1438-55. 2011.... - Neutralization of granulocyte macrophage colony-stimulating factor decreases amyloid beta 1-42 and suppresses microglial activity in a transgenic mouse model of Alzheimer's diseaseMaria Manczak
Oregon National Primate Research Center, Beaverton, 97006, USA
Hum Mol Genet 18:3876-93. 2009..These findings indicating the ability of the anti-GM-CSF antibody to reduce Abeta1-42 and microglial activity in Tg2576 mice may have therapeutic implications for Alzheimer's disease... - Time-course of mitochondrial gene expressions in mice brains: implications for mitochondrial dysfunction, oxidative damage, and cytochrome c in agingMaria Manczak
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
J Neurochem 92:494-504. 2005.... - Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's diseaseMarcus J Calkins
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA
Hum Mol Genet 20:4515-29. 2011.... - Toxicity of neurons treated with herbicides and neuroprotection by mitochondria-targeted antioxidant SS31Tejaswini P Reddy
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Int J Environ Res Public Health 8:203-21. 2011..Based on these results, we propose that herbicides--picloram and triclopyr appear to damage neurons, and the SS31 peptide appears to protect neurons from herbicide toxicity... - Mitochondria-targeted catalase reduces abnormal APP processing, amyloid β production and BACE1 in a mouse model of Alzheimer's disease: implications for neuroprotection and lifespan extensionPeizhong Mao
Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW185th Avenue, Beaverton, OR 97006, USA
Hum Mol Genet 21:2973-90. 2012..These findings indicate that mitochondria-targeted molecules may be an effective therapeutic approach to treat patients with AD... - Differential expression of oxidative phosphorylation genes in patients with Alzheimer's disease: implications for early mitochondrial dysfunction and oxidative damageMaria Manczak
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR, USA
Neuromolecular Med 5:147-62. 2004..Based on these results, we propose that an increase in cytochrome oxidase gene expression might be the result of functional compensation by the surviving neurons or an early mitochondrial alteration related to increased oxidative damage... - Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progressionMaria Manczak
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Aveue, Beaverton, 97006, USA
Hum Mol Genet 15:1437-49. 2006..These findings suggest that early mitochondrially targeted therapeutic interventions may be effective in delaying AD progression in elderly individuals and in treating AD patients... - Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damageMaria Manczak
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Hum Mol Genet 20:2495-509. 2011..Inhibiting, these abnormal interactions may be a therapeutic strategy to reduce mitochondrial fragmentation, neuronal and synaptic damage and cognitive decline in patients with AD... - Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons: implications for mitochondrial dysfunction and neuronal damageMaria Manczak
Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health and Science University, Beaverton, OR 97006, USA
Hum Mol Genet 21:2538-47. 2012.... - CART peptide is a potential endogenous antioxidant and preferentially localized in mitochondriaPeizhong Mao
The Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon, United States of America
PLoS ONE 7:e29343. 2012..We further propose that it may have strong therapeutic properties for human diseases in which oxidative stress is strongly involved such as Parkinson's disease... - Amyloid precursor protein-mediated free radicals and oxidative damage: implications for the development and progression of Alzheimer's diseaseP Hemachandra Reddy
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006, USA
J Neurochem 96:1-13. 2006.... - Dynamin-related protein 1 heterozygote knockout mice do not have synaptic and mitochondrial deficienciesMaria Manczak
Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1822:862-74. 2012..These findings suggest that partial Drp1 reduction does not affect mitochondrial and synaptic viability and may have therapeutic use in treating patients with Alzheimer's disease and Huntington's disease... - Mitochondrial DNA deletions and differential mitochondrial DNA content in Rhesus monkeys: implications for agingPeizhong Mao
Neuroscience Division, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1822:111-9. 2012.... - Amyloid beta impairs mitochondrial anterograde transport and degenerates synapses in Alzheimer's disease neuronsMarcus J Calkins
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1812:507-13. 2011..These findings suggest that, in neurons affected by AD, Aβ is toxic, impairs mitochondrial movements, reduces mitochondrial length, and causes synaptic degeneration... - Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: implications for early intervention and therapeuticsPeizhong Mao
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1812:1359-70. 2011..It also discusses the therapeutic approaches against oxidative DNA damage and treatment strategies in AD... - A transgenic mouse model for Alzheimer's disease has impaired synaptic gain but normal synaptic dynamicsUlises M Ricoy
Department of Behavioral Neuroscience, Oregon Health and Science University, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239, United States
Neurosci Lett 500:212-5. 2011..We conclude that the chronic accumulation of Aβ impairs synaptic transmission through a reduction in the synaptic gain, while preserving the synaptic dynamics... - Role of mitochondria in neurodegenerative diseases: mitochondria as a therapeutic target in Alzheimer's diseaseP Hemachandra Reddy
Division of Neuroscience, Oregon National Primate Research Center, Beaverton, USA
CNS Spectr 14:8-13; discussion 16-8. 2009.... - Assessment of newly synthesized mitochondrial DNA using BrdU labeling in primary neurons from Alzheimer's disease mice: Implications for impaired mitochondrial biogenesis and synaptic damageMarcus J Calkins
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1812:1182-9. 2011..These findings suggest that Aβ and mitochondrial toxins enhance mitochondrial fragmentation in the cell body, and may cause impaired axonal transport of mitochondria leading to synaptic degeneration... - Interaction of the nuclear matrix protein NAKAP with HypA and huntingtin: implications for nuclear toxicity in Huntington's disease pathogenesisJonathan A Sayer
Neurological Sciences Institute, Oregon Health and Science University, Beaverton, OR 97006, USA
Neuromolecular Med 7:297-310. 2005..Hence, the NAKAP-HypA scaffold is a potential nuclear docking site for huntingtin protein and may contribute to the nuclear accumulation of huntingtin observed in HD... - Can herbs provide a new generation of drugs for treating Alzheimer's disease?Thimmappa S Anekonda
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Brain Res Brain Res Rev 50:361-76. 2005..The chemical compositions of herbs and their potential for alleviating or reducing symptoms of AD or for affecting the disease mechanism need to be further studied... - The use of real-time PCR analysis in a gene expression study of Alzheimer's disease post-mortem brainsRamana V Gutala
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, OR 97006, USA
J Neurosci Methods 132:101-7. 2004..A comparative gene expression analysis also suggests that synaptophysin is down-regulated in AD brain specimens compared to control brain specimens... - Neuronal protection by sirtuins in Alzheimer's diseaseThimmappa S Anekonda
Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006, USA
J Neurochem 96:305-13. 2006..In this review, we discuss the possible mechanisms of sirtuins involved in neuronal protection and the potential therapeutic value of sirtuins in healthy aging and AD... - Is multiple sclerosis a mitochondrial disease?Peizhong Mao
Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
Biochim Biophys Acta 1802:66-79. 2010..In this article, we also focus on the mechanisms of mitochondrial dysfunction that are involved in MS, including mitochondrial DNA defects, and mitochondrial structural/functional changes... - Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's diseaseMaria Manczak
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA
Hum Mol Genet 21:5131-46. 2012....
Research Grants
- Microarrays for Alzheimer's Disease Mouse ModelsP Reddy; Fiscal Year: 2003..The outcome of this proposed investigation will be useful in screening several mitochondrial antioxidants in AD transgenic mouse models as pre-clinical trials of AD patients...
- Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's DiseaseP Hemachandra Reddy; Fiscal Year: 2007..Aim 3 will provide a mechanistic test of the hypothesis by characterizing neuroprotective mechanisms of mitochondrial oxidative damage, and will take us closer to identifying novel therapies of AD. ..
- Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's DiseaseP Hemachandra Reddy; Fiscal Year: 2009..Aim 3 will provide a mechanistic test of the hypothesis by characterizing neuroprotective mechanisms of mitochondrial oxidative damage, and will take us closer to identifying novel therapies of AD. ..
- ABETA TOXICITY, ROS AND MITOCHONDRIAL DYSFUNCTION IN AGING/ALZHEIMER'S DISEASEP Hemachandra Reddy; Fiscal Year: 2010..Aim 3 will provide a mechanistic test of the hypothesis by characterizing neuroprotective mechanisms of mitochondrial oxidative damage, and will take us closer to identifying novel therapies of AD. ..