P Hemachandra Reddy

Summary

Affiliation: Oregon Health and Science University
Country: USA

Publications

  1. pmc Amyloid beta-induced glycogen synthase kinase 3β phosphorylated VDAC1 in Alzheimer's disease: implications for synaptic dysfunction and neuronal damage
    P 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 Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA Electronic address
    Biochim Biophys Acta 1832:1913-21. 2013
  2. pmc 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
  3. pmc Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer's disease: implications to mitochondria-targeted antioxidant therapeutics
    P 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
  4. pmc Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's disease
    P 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
  5. ncbi request reprint Mapping cellular transcriptosomes in autopsied Alzheimer's disease subjects and relevant animal models
    P 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
  6. pmc Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's disease
    P Hemachandra Reddy
    Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, 97006, USA
    Exp Neurol 218:286-92. 2009
  7. pmc Mitochondrial structural and functional dynamics in Huntington's disease
    P 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
  8. pmc Granulocyte-macrophage colony-stimulating factor antibody suppresses microglial activity: implications for anti-inflammatory effects in Alzheimer's disease and multiple sclerosis
    P 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
  9. ncbi request reprint 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 disease
    P Hemachandra Reddy
    Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, OR 97006, USA
    Hum Mol Genet 13:1225-40. 2004
  10. pmc Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline
    P Hemachandra Reddy
    Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Beaverton, OR, USA
    J Alzheimers Dis 20:S499-512. 2010

Collaborators

Detail Information

Publications50

  1. pmc Amyloid beta-induced glycogen synthase kinase 3β phosphorylated VDAC1 in Alzheimer's disease: implications for synaptic dysfunction and neuronal damage
    P 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 Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA Electronic address
    Biochim Biophys Acta 1832:1913-21. 2013
    ..We discuss the involvement of GSK3β in the phosphorylation of VDAC1 and dissociation of VADC1 with hexokinases in AD neurons. ..
  2. pmc 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...
  3. pmc Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer's disease: implications to mitochondria-targeted antioxidant therapeutics
    P 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...
  4. pmc Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's disease
    P 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...
  5. ncbi request reprint Mapping cellular transcriptosomes in autopsied Alzheimer's disease subjects and relevant animal models
    P 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...
  6. pmc Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's disease
    P 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...
  7. pmc Mitochondrial structural and functional dynamics in Huntington's disease
    P 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...
  8. pmc Granulocyte-macrophage colony-stimulating factor antibody suppresses microglial activity: implications for anti-inflammatory effects in Alzheimer's disease and multiple sclerosis
    P 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)...
  9. ncbi request reprint 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 disease
    P 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...
  10. pmc Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline
    P 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...
  11. pmc Dynamin-related protein 1 and mitochondrial fragmentation in neurodegenerative diseases
    P 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
    ....
  12. pmc Mitochondria as a therapeutic target for aging and neurodegenerative diseases
    P 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...
  13. pmc Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's disease
    P 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...
  14. pmc Mitochondrial medicine for aging and neurodegenerative diseases
    P 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
    ....
  15. pmc Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease
    P 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...
  16. ncbi request reprint Mitochondrial dysfunction in aging and Alzheimer's disease: strategies to protect neurons
    P 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...
  17. ncbi request reprint Differential loss of synaptic proteins in Alzheimer's disease: implications for synaptic dysfunction
    P 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...
  18. ncbi request reprint 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...
  19. pmc RNA silencing of genes involved in Alzheimer's disease enhances mitochondrial function and synaptic activity
    Maria Manczak
    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 1832:2368-78. 2013
    ..Thus, these findings also suggest that the reduction of APP, Tau, and VDAC1 mRNA expressions may have therapeutic value for patients with AD. ..
  20. pmc Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's disease
    Ulziibat 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
    ....
  21. pmc Mitochondria-targeted antioxidants protect against amyloid-beta toxicity in Alzheimer's disease neurons
    Maria 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...
  22. pmc Toxicity of neurons treated with herbicides and neuroprotection by mitochondria-targeted antioxidant SS31
    Tejaswini 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...
  23. pmc Neutralization of granulocyte macrophage colony-stimulating factor decreases amyloid beta 1-42 and suppresses microglial activity in a transgenic mouse model of Alzheimer's disease
    Maria 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...
  24. pmc Abnormal mitochondrial dynamics, mitochondrial loss and mutant huntingtin oligomers in Huntington's disease: implications for selective neuronal damage
    Ulziibat 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
    ....
  25. ncbi request reprint Time-course of mitochondrial gene expressions in mice brains: implications for mitochondrial dysfunction, oxidative damage, and cytochrome c in aging
    Maria 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
    ....
  26. pmc Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease
    Marcus 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
    ....
  27. pmc 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 extension
    Peizhong 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...
  28. ncbi request reprint Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression
    Maria 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...
  29. ncbi request reprint Differential expression of oxidative phosphorylation genes in patients with Alzheimer's disease: implications for early mitochondrial dysfunction and oxidative damage
    Maria 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...
  30. pmc MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis
    Peizhong Mao
    Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA
    Biochim Biophys Acta 1832:2322-31. 2013
    ..These protective effects are likely via multiple mechanisms, including the attenuation of the robust immune response. These results suggest that MitoQ may be a new candidate for the treatment of MS. ..
  31. pmc Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage
    Maria 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...
  32. pmc Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons: implications for mitochondrial dysfunction and neuronal damage
    Maria 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
    ....
  33. pmc CART peptide is a potential endogenous antioxidant and preferentially localized in mitochondria
    Peizhong 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...
  34. ncbi request reprint Amyloid precursor protein-mediated free radicals and oxidative damage: implications for the development and progression of Alzheimer's disease
    P Hemachandra Reddy
    Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon 97006, USA
    J Neurochem 96:1-13. 2006
    ....
  35. doi request reprint Abnormal interaction of oligomeric amyloid-β with phosphorylated tau: implications to synaptic dysfunction and neuronal damage
    Maria Manczak
    Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA
    J Alzheimers Dis 36:285-95. 2013
    ..Our findings suggest that binding sites between Aβ and phosphorylated tau need to be identified and molecules developed to inhibit this interaction...
  36. pmc Dynamin-related protein 1 heterozygote knockout mice do not have synaptic and mitochondrial deficiencies
    Maria 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...
  37. pmc Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's disease
    Maria 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
    ....
  38. pmc Mitochondrial DNA deletions and differential mitochondrial DNA content in Rhesus monkeys: implications for aging
    Peizhong 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
    ....
  39. pmc Amyloid beta impairs mitochondrial anterograde transport and degenerates synapses in Alzheimer's disease neurons
    Marcus 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...
  40. pmc Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: implications for early intervention and therapeutics
    Peizhong 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...
  41. pmc A transgenic mouse model for Alzheimer's disease has impaired synaptic gain but normal synaptic dynamics
    Ulises 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...
  42. ncbi request reprint Interaction of the nuclear matrix protein NAKAP with HypA and huntingtin: implications for nuclear toxicity in Huntington's disease pathogenesis
    Jonathan 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...
  43. pmc Role of mitochondria in neurodegenerative diseases: mitochondria as a therapeutic target in Alzheimer's disease
    P Hemachandra Reddy
    Division of Neuroscience, Oregon National Primate Research Center, Beaverton, USA
    CNS Spectr 14:8-13; discussion 16-8. 2009
    ....
  44. pmc Assessment of newly synthesized mitochondrial DNA using BrdU labeling in primary neurons from Alzheimer's disease mice: Implications for impaired mitochondrial biogenesis and synaptic damage
    Marcus 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...
  45. ncbi request reprint 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...
  46. ncbi request reprint Neuronal protection by sirtuins in Alzheimer's disease
    Thimmappa 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...
  47. pmc 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...
  48. ncbi request reprint The use of real-time PCR analysis in a gene expression study of Alzheimer's disease post-mortem brains
    Ramana 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...
  49. ncbi request reprint Reduced VDAC1 protects against Alzheimer's disease, mitochondria, and synaptic deficiencies
    Maria Manczak
    Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR, USA
    J Alzheimers Dis 37:679-90. 2013
    ..These findings suggest that reduced VDAC1 expression, such as that we found in the VDAC1+/- mice, may be beneficial to synaptic activity, may improve function, and may protect against toxicities of AD-related genes. ..

Research Grants5

  1. Microarrays for Alzheimer's Disease Mouse Models
    P 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...
  2. Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's Disease
    P 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. ..
  3. Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's Disease
    P 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. ..
  4. ABETA TOXICITY, ROS AND MITOCHONDRIAL DYSFUNCTION IN AGING/ALZHEIMER'S DISEASE
    P 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. ..