T G Beach

Summary

Affiliation: Sun Health Research Institute
Country: USA

Publications

  1. ncbi request reprint Cholinergic deafferentation of the rabbit cortex: a new animal model of Abeta deposition
    T G Beach
    Sun Health Research Institute, Sun City, AZ 85351, USA
    Neurosci Lett 283:9-12. 2000
  2. ncbi request reprint Reduction of cortical amyloid beta levels in guinea pig brain after systemic administration of physostigmine
    T G Beach
    Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85372, USA
    Neurosci Lett 310:21-4. 2001
  3. ncbi request reprint Muscarinic agonists as preventative therapy for Alzheimer's disease
    Thomas G Beach
    Sun Health Research Institute, 10515 Santa Fe Drive, Sun City, AZ 85372, USA
    Curr Opin Investig Drugs 3:1633-6. 2002
  4. ncbi request reprint Cortical cholinergic denervation elicits vascular A beta deposition
    A E Roher
    Sun Health Research Institute, Sun City, Arizona 85351, USA
    Ann N Y Acad Sci 903:366-73. 2000
  5. pmc The evolution of A beta peptide burden in the APP23 transgenic mice: implications for A beta deposition in Alzheimer disease
    Y M Kuo
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, Arizona 85351, USA
    Mol Med 7:609-18. 2001
  6. ncbi request reprint Reduction of cerebrospinal fluid amyloid beta after systemic administration of M1 muscarinic agonists
    T G Beach
    Sun Health Research Institute, 10515 Santa Fe Drive, Sun City, AZ 85372, USA
    Brain Res 905:220-3. 2001
  7. ncbi request reprint Involvement of microglial receptor for advanced glycation endproducts (RAGE) in Alzheimer's disease: identification of a cellular activation mechanism
    L F Lue
    The Roberts Alzheimer s Disease Center, Sun Health Research Institute, Sun City, Arizona 85372, USA
    Exp Neurol 171:29-45. 2001
  8. ncbi request reprint Comparative analysis of amyloid-beta chemical structure and amyloid plaque morphology of transgenic mouse and Alzheimer's disease brains
    Y M Kuo
    Longtine Center for Molecular Biology and Genetics and the Civin Laboratory of Neuropathology, Sun Health Research Institute, Sun City, Arizona 85351, USA
    J Biol Chem 276:12991-8. 2001
  9. doi request reprint Pathologic findings in prospectively ascertained essential tremor subjects
    H A Shill
    Sun Health Research Institute, Sun City, AZ, USA
    Neurology 70:1452-5. 2008
  10. pmc Functional, global and cognitive decline correlates to accumulation of Alzheimer's pathology in MCI and AD
    M N Sabbagh
    The Cleo Roberts Center, Banner Sun Health Research Institute, 10515 W Santa Fe Dr Sun City, AZ 85351, USA
    Curr Alzheimer Res 7:280-6. 2010

Detail Information

Publications45

  1. ncbi request reprint Cholinergic deafferentation of the rabbit cortex: a new animal model of Abeta deposition
    T G Beach
    Sun Health Research Institute, Sun City, AZ 85351, USA
    Neurosci Lett 283:9-12. 2000
    ..Biochemical measurements confirmed that lesioned animals had 2.5- and 8-fold elevations of cortical Abeta40 and Abeta42, respectively. Cholinergic deafferentation may be one factor that can contribute to Abeta deposition...
  2. ncbi request reprint Reduction of cortical amyloid beta levels in guinea pig brain after systemic administration of physostigmine
    T G Beach
    Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85372, USA
    Neurosci Lett 310:21-4. 2001
    ..Levels of cortical beta-amyloid precursor protein were not significantly affected by drug treatment. These results suggest that cholinergic therapy may affect the course of AD by limiting Abeta accumulation...
  3. ncbi request reprint Muscarinic agonists as preventative therapy for Alzheimer's disease
    Thomas G Beach
    Sun Health Research Institute, 10515 Santa Fe Drive, Sun City, AZ 85372, USA
    Curr Opin Investig Drugs 3:1633-6. 2002
    ..Muscarinic agonists, particularly M1-selective agents, have been shown to decrease the production of Abeta in vitro and in vivo; these compounds may be uniquely suited to a preventative role in AD therapy...
  4. ncbi request reprint Cortical cholinergic denervation elicits vascular A beta deposition
    A E Roher
    Sun Health Research Institute, Sun City, Arizona 85351, USA
    Ann N Y Acad Sci 903:366-73. 2000
    ....
  5. pmc The evolution of A beta peptide burden in the APP23 transgenic mice: implications for A beta deposition in Alzheimer disease
    Y M Kuo
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, Arizona 85351, USA
    Mol Med 7:609-18. 2001
    ..Both Tg mice reflect decreased A beta elimination and as models for the amyloid cascade they are useful to study AD pathophysiology and therapy...
  6. ncbi request reprint Reduction of cerebrospinal fluid amyloid beta after systemic administration of M1 muscarinic agonists
    T G Beach
    Sun Health Research Institute, 10515 Santa Fe Drive, Sun City, AZ 85372, USA
    Brain Res 905:220-3. 2001
    ..Rabbits treated for 5 days with s.c. injections of each drug (2 mg/kg/day) had levels of CSF A beta which were between 55 and 71% of control for A beta 1-40 and between 59 and 84% of control for A beta 1--42...
  7. ncbi request reprint Involvement of microglial receptor for advanced glycation endproducts (RAGE) in Alzheimer's disease: identification of a cellular activation mechanism
    L F Lue
    The Roberts Alzheimer s Disease Center, Sun Health Research Institute, Sun City, Arizona 85372, USA
    Exp Neurol 171:29-45. 2001
    ..These data suggest a positive feedback loop in which Abeta-RAGE-mediated microglial activation enhances expression of M-CSF and RAGE, possibly initiating an ascending spiral of cellular activation...
  8. ncbi request reprint Comparative analysis of amyloid-beta chemical structure and amyloid plaque morphology of transgenic mouse and Alzheimer's disease brains
    Y M Kuo
    Longtine Center for Molecular Biology and Genetics and the Civin Laboratory of Neuropathology, Sun Health Research Institute, Sun City, Arizona 85351, USA
    J Biol Chem 276:12991-8. 2001
    ..The appraisal of therapeutic agents or protocols in these animal models must be judged in the context of the lack of complete equivalence between the transgenic mouse plaques and the human AD lesions...
  9. doi request reprint Pathologic findings in prospectively ascertained essential tremor subjects
    H A Shill
    Sun Health Research Institute, Sun City, AZ, USA
    Neurology 70:1452-5. 2008
    ..To assess pathologic changes in prospectively characterized subjects with essential tremor (ET)...
  10. pmc Functional, global and cognitive decline correlates to accumulation of Alzheimer's pathology in MCI and AD
    M N Sabbagh
    The Cleo Roberts Center, Banner Sun Health Research Institute, 10515 W Santa Fe Dr Sun City, AZ 85351, USA
    Curr Alzheimer Res 7:280-6. 2010
    ..Cognitive, global and functional instruments have been extensively investigated for correlations with neuropathological changes such as neurofibrillary tangles (NFTs), plaques, and synapse loss in the brain...
  11. ncbi request reprint Gene expression profiling of amyloid beta peptide-stimulated human post-mortem brain microglia
    D G Walker
    Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Neurobiol Aging 22:957-66. 2001
    ..These results confirm the usefulness of the gene array approach for studying Abeta-mediated inflammatory processes...
  12. ncbi request reprint Pathologic and nicotinic receptor binding differences between mild cognitive impairment, Alzheimer disease, and normal aging
    Marwan N Sabbagh
    Cleo Roberts Center for Clinical Research, Sun Health Research Institute, Sun City, AZ 85351, USA
    Arch Neurol 63:1771-6. 2006
    ..Decreased neocortical nicotinic receptor binding is characteristic of AD but has not been investigated in subjects with MCI...
  13. ncbi request reprint Alzheimer's disease a century later
    Richard J Caselli
    Department of Neurology, Mayo Clinic and Arizona Alzheimer s Disease Consortium, Scottsdale 85259, USA
    J Clin Psychiatry 67:1784-800. 2006
    ..To provide a current survey of the clinical and pathologic features, known genetic and suggested pathogenic contributions, diagnosis, and treatment of Alzheimer's disease (AD) and related forms of dementia...
  14. ncbi request reprint Marked microglial reaction in normal aging human substantia nigra: correlation with extraneuronal neuromelanin pigment deposits
    Thomas G Beach
    Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Acta Neuropathol 114:419-24. 2007
    ....
  15. ncbi request reprint Phenotypic variability associated with progranulin haploinsufficiency in patients with the common 1477C-->T (Arg493X) mutation: an international initiative
    Rosa Rademakers
    Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA
    Lancet Neurol 6:857-68. 2007
    ..The most common mutation in GRN is Arg493X. We aimed to establish the contribution of this mutation to FTLD and related disorders...
  16. pmc Gene expression profiles in anatomically and functionally distinct regions of the normal aged human brain
    Winnie S Liang
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ 85004, USA
    Physiol Genomics 28:311-22. 2007
    ..These neuronal profiles will provide valuable reference information for future studies of the brain, in normal aging, AD and other neurological and psychiatric disorders...
  17. pmc Altered neuronal gene expression in brain regions differentially affected by Alzheimer's disease: a reference data set
    Winnie S Liang
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona 85004, USA
    Physiol Genomics 33:240-56. 2008
    ..We provide this carefully phenotyped, laser capture microdissected intraindividual brain region expression data set to the community as a public resource...
  18. pmc Presenilin-1 280Glu-->Ala mutation alters C-terminal APP processing yielding longer abeta peptides: implications for Alzheimer's disease
    Gregory D Van Vickle
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, Arizona 85351, USA
    Mol Med 14:184-94. 2008
    ....
  19. doi request reprint Physiologic origins of age-related beta-amyloid deposition
    Thomas G Beach
    Sun Health Research Institute, Sun City, Ariz 85351, USA
    Neurodegener Dis 5:143-5. 2008
    ..Brain beta-amyloid (Abeta) deposition is an extremely common accompaniment of aging in humans and many other mammalian species. We hypothesized that normal physiological changes of aging cause Abeta deposition...
  20. pmc The Sun Health Research Institute Brain Donation Program: description and experience, 1987-2007
    Thomas G Beach
    Sun Health Research Institute, Sun City, 85351, USA
    Cell Tissue Bank 9:229-45. 2008
    ....
  21. pmc Tg-SwDI transgenic mice exhibit novel alterations in AbetaPP processing, Abeta degradation, and resilient amyloid angiopathy
    Gregory D Van Vickle
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, AZ 85351, USA
    Am J Pathol 173:483-93. 2008
    ....
  22. pmc Evaluation of alpha-synuclein immunohistochemical methods used by invited experts
    Thomas G Beach
    Civin Laboratory for Neuropathology, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Acta Neuropathol 116:277-88. 2008
    ..Some methods, however, achieved relatively high sensitivities with optimized formic acid protocols combined with a hydrolytic step. One method was developed that allows high sensitivity with commercially available reagents...
  23. ncbi request reprint Circle of Willis atherosclerosis: association with Alzheimer's disease, neuritic plaques and neurofibrillary tangles
    Thomas G Beach
    W H Civin Laboratory for Neuropathology, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Acta Neuropathol 113:13-21. 2007
    ..The results suggest that the statistical association between intracranial atherosclerosis and AD is not an artifact of diagnostic misclassification or of unequal distribution of the apolipoprotein E-epsilon4 allele...
  24. ncbi request reprint Interaction of cardiovascular disease and neurodegeneration: transcranial Doppler ultrasonography and Alzheimer's disease
    Alex E Roher
    Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City AZ 85351, USA
    Neurol Res 28:672-8. 2006
    ..In this study, we examine the arteries of the circle of Willis by transcranial Doppler (TCD) ultrasonography...
  25. ncbi request reprint Thiorphan-induced neprilysin inhibition raises amyloid beta levels in rabbit cortex and cerebrospinal fluid
    Amanda J Newell
    Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Neurosci Lett 350:178-80. 2003
    ..Results for Abeta42 showed a similar trend. The results indicate that age-related decreases of neprilysin could lead to increased brain concentrations of Abeta, plaque formation, and AD...
  26. ncbi request reprint Hippocampal sclerosis dementia with tauopathy
    Thomas G Beach
    W H Civin Laboratory for Neuropathology, Sun Health Research Institute, Sun City, Ariz 85372, USA
    Brain Pathol 13:263-78. 2003
    ..The results suggest that most cases of HS dementia are sporadic multisystem tauopathies; we suggest the term "hippocampal sclerosis dementia with tauopathy" (HSDT) for these...
  27. ncbi request reprint Circle of willis atherosclerosis is a risk factor for sporadic Alzheimer's disease
    Alex E Roher
    Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, 10515 W Santa Fe Dr, Sun City, AZ 85351, USA
    Arterioscler Thromb Vasc Biol 23:2055-62. 2003
    ..We conducted a quantitative investigation of brain arterial atherosclerotic damage and its relationship to sporadic Alzheimer's disease (AD)...
  28. ncbi request reprint Substantia nigra Marinesco bodies are associated with decreased striatal expression of dopaminergic markers
    Thomas G Beach
    Sun Health Research Institute, Sun City, Arizona 85372, USA
    J Neuropathol Exp Neurol 63:329-37. 2004
    ..Further studies are needed to ascertain the molecular basis of Marinesco body formation; preliminary studies indicate that proteasome dysfunction can lead to similar abnormalities in cultured cells...
  29. ncbi request reprint Atherosclerosis, vascular amyloidosis and brain hypoperfusion in the pathogenesis of sporadic Alzheimer's disease
    Walter Kalback
    Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, AZ, USA
    Neurol Res 26:525-39. 2004
    ..Our data strongly suggest that severe hemodynamic disturbances contribute to sporadic AD and support the numerous observations indicating cardiovascular system participation in the pathogenesis of these dementias...
  30. ncbi request reprint Atherosclerosis of cerebral arteries in Alzheimer disease
    Alex E Roher
    Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, Ariz 85351, USA
    Stroke 35:2623-7. 2004
    ..Confirmation of a central role for vascular pathology in AD will suggest important treatment options and directions for additional interventions to stave off this dementia...
  31. ncbi request reprint Increased expression of the urokinase plasminogen-activator receptor in amyloid beta peptide-treated human brain microglia and in AD brains
    Douglas G Walker
    Civin Laboratory of Neuropathology, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
    Brain Res 926:69-79. 2002
    ..These results provide a connection between the induction of oxidative stress in AD and microglial activation, and establish a possible involvement of uPAR in AD pathogenesis...
  32. ncbi request reprint An association with great implications: vascular pathology and Alzheimer disease
    Alex E Roher
    Alzheimer Dis Assoc Disord 20:73-5. 2006
  33. pmc Amyloid-beta peptide remnants in AN-1792-immunized Alzheimer's disease patients: a biochemical analysis
    R Lyle Patton
    The Longtine Center for Molecular Biology and Genetics, W H Civin Laboratory for Neuropathology, M D Sun Health Research Institute, 10515 W Santa Fe Dr, Sun City, AZ 85351, USA
    Am J Pathol 169:1048-63. 2006
    ..This may allow Abeta mobilization under conditions in which drainage and degradation of these toxic peptides is efficient...
  34. pmc Cortical and leptomeningeal cerebrovascular amyloid and white matter pathology in Alzheimer's disease
    Alex E Roher
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, AZ 85351, USA
    Mol Med 9:112-22. 2003
    ..This failure of fluid drainage has implications for therapeutic strategies to treat Alzheimer's disease...
  35. pmc Phosphorylated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Masato Hasegawa
    Department of Molecular Neurobiology, Tokyo Institute of Psychiatry, Tokyo Metropolitan Organization for Medical Research, Kamikitazawa, Setagaya Ku, Tokyo, Japan
    Ann Neurol 64:60-70. 2008
    ..The aim of this study was to identify the phosphorylation sites and responsible kinases, and to clarify the pathological significance of phosphorylation of TDP-43...
  36. ncbi request reprint Myoclonus in Lewy body disorders
    John N Caviness
    Department of Neurology, Mayo Clinic Scottsdale, Scottsdale, Arizona, USA
    Adv Neurol 89:23-30. 2002
  37. ncbi request reprint Progressive aphasia with Lewy bodies
    Richard J Caselli
    Department of Neurology, Mayo Clinic Scottsdale, 13400 East Shea Boulevard, AZ 85259, USA
    Dement Geriatr Cogn Disord 14:55-8. 2002
    ....
  38. ncbi request reprint Small-amplitude cortical myoclonus in Parkinson's disease: physiology and clinical observations
    John N Caviness
    Parkinson s Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259, USA
    Mov Disord 17:657-62. 2002
    ..Although the myoclonus occurred without dementia in these cases, its relationship to the subsequent development of cognitive impairment remains to be defined...
  39. pmc Alzheimer's disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons
    Winnie S Liang
    Neurogenomics Division, Translational Genomics Research Institute, 445 North Fifth Street, Phoenix, AZ 85004, USA
    Proc Natl Acad Sci U S A 105:4441-6. 2008
    ..Cerebral metabolic rate for glucose abnormalities in FDG PET studies of AD may be associated with reduced neuronal expression of nuclear genes encoding subunits of the mitochondrial electron transport chain...
  40. ncbi request reprint Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration
    Jennifer Gass
    Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    Hum Mol Genet 15:2988-3001. 2006
    ..Neuropathological examination showed FTLD with ubiquitin-positive cytoplasmic and intranuclear inclusions in all PGRN mutation carriers...
  41. ncbi request reprint TgCRND8 amyloid precursor protein transgenic mice exhibit an altered gamma-secretase processing and an aggressive, additive amyloid pathology subject to immunotherapeutic modulation
    Gregory D Van Vickle
    The Longtine Center for Molecular Biology and Genetics, Sun Health Research Institute, Sun City, Arizona 85351, USA
    Biochemistry 46:10317-27. 2007
    ..However, given the phylogenetic distance and the differences in APP processing and Abeta chemistry between Tg mice and AD, caution should be applied in projecting mouse therapeutic interventions onto human subjects...
  42. ncbi request reprint A high-density whole-genome association study reveals that APOE is the major susceptibility gene for sporadic late-onset Alzheimer's disease
    Keith D Coon
    Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Ariz 85004, USA
    J Clin Psychiatry 68:613-8. 2007
    ....
  43. pmc Alterations in immunological and neurological gene expression patterns in Alzheimer's disease tissues
    Ashani T Weeraratna
    Laboratory of Immunology, National Institutes of Health, Baltimore, MD 21224, USA
    Exp Cell Res 313:450-61. 2007
    ..Together, these findings open up new avenues of investigation and possible therapeutic strategies targeting inflammation and amyloid clearance in AD patients...
  44. pmc Gene expression correlates of neurofibrillary tangles in Alzheimer's disease
    Travis Dunckley
    Neurogenomics Division, Translational Genomics Research Institute, 445 North 5th Street, Phoenix, AZ 85004, USA
    Neurobiol Aging 27:1359-71. 2006
    ..Functional validation studies are underway to determine which candidate genes may be causally related to NFT neuropathology, thus providing therapeutic targets for the treatment of AD...
  45. pmc Cholesterol retention in Alzheimer's brain is responsible for high beta- and gamma-secretase activities and Abeta production
    Huaqi Xiong
    Neurobiology Program, Institute for Biological Sciences, National Research Council of Canada, Ottawa, Canada
    Neurobiol Dis 29:422-37. 2008
    ....