Thomas M Wisniewski

Summary

Affiliation: New York University
Country: USA

Publications

  1. ncbi request reprint Immunization treatment approaches in Alzheimer's and prion diseases
    Thomas Wisniewski
    Department of Neurology, New York University Medical Center, Millhauser Laboratory, HN419, 550 First Avenue, New York, NY 10016, USA
    Curr Neurol Neurosci Rep 2:400-4. 2002
  2. ncbi request reprint Intraneuronal Abeta42 accumulation in Down syndrome brain
    Chica Mori
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Amyloid 9:88-102. 2002
  3. ncbi request reprint Is vaccination against transmissible spongiform encephalopathy feasible?
    T Wisniewski
    Department of Psychiatry, New York University School of Medicine, 560 First Avenue, New York, NY 10016, USA
    Rev Sci Tech 26:243-51. 2007
  4. ncbi request reprint Therapeutic approaches for prion and Alzheimer's diseases
    Thomas Wisniewski
    Department of Neurology, New York University School of Medicine, NY 10016, USA
    FEBS J 274:3784-98. 2007
  5. ncbi request reprint Immunological and anti-chaperone therapeutic approaches for Alzheimer disease
    Thomas Wisniewski
    Department of Neurology, New York University School of Medicine, 550 First Avenue, NewYork, NY 10016, USA
    Brain Pathol 15:72-7. 2005
  6. ncbi request reprint Vaccines for conformational disorders
    Marcin Sadowski
    Department of Neurology, New York University School of Medicine, 550 First Avenue, MHL Rm HN 419, New York, NY 10016, USA
    Expert Rev Vaccines 3:279-90. 2004
  7. ncbi request reprint Therapeutics in Alzheimer's and prion diseases
    T Wisniewski
    Department of Neurology, New York University Medical Center, 550 First Avenue TH 427, New York, NY 10016, USA
    Biochem Soc Trans 30:574-8. 2002
  8. pmc High titers of mucosal and systemic anti-PrP antibodies abrogate oral prion infection in mucosal-vaccinated mice
    F Goni
    Department of Neurology, New York University School of Medicine, New York, NY 10016, USA
    Neuroscience 153:679-86. 2008
  9. ncbi request reprint Melatonin reverses the profibrillogenic activity of apolipoprotein E4 on the Alzheimer amyloid Abeta peptide
    B Poeggeler
    University of South Alabama, Mobile, Alabama 36688, New York University, New York, New York 10003, USA
    Biochemistry 40:14995-5001. 2001
  10. ncbi request reprint Reversion of prion protein conformational changes by synthetic beta-sheet breaker peptides
    C Soto
    New York University Medical Center, NY, USA
    Lancet 355:192-7. 2000

Research Grants

  1. Immunization Approaches for Alzheimer's Disease
    Thomas Wisniewski; Fiscal Year: 2007

Collaborators

Detail Information

Publications29

  1. ncbi request reprint Immunization treatment approaches in Alzheimer's and prion diseases
    Thomas Wisniewski
    Department of Neurology, New York University Medical Center, Millhauser Laboratory, HN419, 550 First Avenue, New York, NY 10016, USA
    Curr Neurol Neurosci Rep 2:400-4. 2002
    ..These immune-based treatment approaches have great potential as rational therapies for this devastating group of disorders, but additional development is needed before they can be safely applied to humans...
  2. ncbi request reprint Intraneuronal Abeta42 accumulation in Down syndrome brain
    Chica Mori
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Amyloid 9:88-102. 2002
    ..We conclude that Abeta42 accumulates intracellularly prior to extracellular Abeta deposition in Down syndrome, and that subsequent maturation of extracellular Abeta deposits elicits inflammatory responses andprecedes NFTs...
  3. ncbi request reprint Is vaccination against transmissible spongiform encephalopathy feasible?
    T Wisniewski
    Department of Psychiatry, New York University School of Medicine, 560 First Avenue, New York, NY 10016, USA
    Rev Sci Tech 26:243-51. 2007
    ....
  4. ncbi request reprint Therapeutic approaches for prion and Alzheimer's diseases
    Thomas Wisniewski
    Department of Neurology, New York University School of Medicine, NY 10016, USA
    FEBS J 274:3784-98. 2007
    ..Therefore, there is a great need for effective therapies for both Alzheimer's disease and prion diseases...
  5. ncbi request reprint Immunological and anti-chaperone therapeutic approaches for Alzheimer disease
    Thomas Wisniewski
    Department of Neurology, New York University School of Medicine, 550 First Avenue, NewYork, NY 10016, USA
    Brain Pathol 15:72-7. 2005
    ..In addition, the recent development of anti-chaperone therapy opens a new therapeutic avenue which is unlikely to be associated with toxicity...
  6. ncbi request reprint Vaccines for conformational disorders
    Marcin Sadowski
    Department of Neurology, New York University School of Medicine, 550 First Avenue, MHL Rm HN 419, New York, NY 10016, USA
    Expert Rev Vaccines 3:279-90. 2004
    ..Novel vaccine strategies are under development for both Alzheimer's disease and prionoses which are predicted to have few or no significant side effects, while being efficacious...
  7. ncbi request reprint Therapeutics in Alzheimer's and prion diseases
    T Wisniewski
    Department of Neurology, New York University Medical Center, 550 First Avenue TH 427, New York, NY 10016, USA
    Biochem Soc Trans 30:574-8. 2002
    ..These conformation-based approaches appear to hold the best promise for therapies for this devastating group of disorders...
  8. pmc High titers of mucosal and systemic anti-PrP antibodies abrogate oral prion infection in mucosal-vaccinated mice
    F Goni
    Department of Neurology, New York University School of Medicine, New York, NY 10016, USA
    Neuroscience 153:679-86. 2008
    ..These promising findings suggest that effective mucosal vaccination is a feasible and useful method for overcoming tolerance to PrP and preventing prion infection via an oral route...
  9. ncbi request reprint Melatonin reverses the profibrillogenic activity of apolipoprotein E4 on the Alzheimer amyloid Abeta peptide
    B Poeggeler
    University of South Alabama, Mobile, Alabama 36688, New York University, New York, New York 10003, USA
    Biochemistry 40:14995-5001. 2001
    ..These findings suggest that reductions in brain melatonin, which occur during aging, may contribute to a proamyloidogenic microenvironment in the aging brain...
  10. ncbi request reprint Reversion of prion protein conformational changes by synthetic beta-sheet breaker peptides
    C Soto
    New York University Medical Center, NY, USA
    Lancet 355:192-7. 2000
    ....
  11. ncbi request reprint Mucosal vaccination delays or prevents prion infection via an oral route
    F Goni
    Department of Neurology, New York University School of Medicine, New York, NY 10016, USA
    Neuroscience 133:413-21. 2005
    ..This promising finding suggests that mucosal vaccination may be a useful method for overcoming tolerance to PrP and preventing prion infection among animal and potentially human populations at risk...
  12. pmc Immunization with a nontoxic/nonfibrillar amyloid-beta homologous peptide reduces Alzheimer's disease-associated pathology in transgenic mice
    E M Sigurdsson
    Department of Neurology, New York University School of Medicine, 550 First Ave, New York, NY 10016, USA
    Am J Pathol 159:439-47. 2001
    ..These promising findings suggest that immunization with nonamyloidogenic Abeta derivatives represents a potentially safer therapeutic approach to reduce amyloid burden in Alzheimer's disease, instead of using toxic Abeta fibrils...
  13. pmc Sodium dodecyl sulfate-resistant complexes of Alzheimer's amyloid beta-peptide with the N-terminal, receptor binding domain of apolipoprotein E
    A A Golabek
    Department of Pathological Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 USA
    Biophys J 79:1008-15. 2000
    ..We propose that the modulation of A beta binding to the N-terminal domain of apoE is a potential therapeutic target for the treatment of amyloidosis-beta...
  14. ncbi request reprint Longitudinal cerebrospinal fluid tau load increases in mild cognitive impairment
    M J de Leon
    Centre for Brain Health, Department of Psychiatry, New York University School of Medicine, NY 10016, USA
    Neurosci Lett 333:183-6. 2002
    ..Longitudinally, only after adjusting for the ventricular volume and only for Ptau231, were increases seen in MCI. Further studies are warranted on mechanisms of tau clearance and on using imaging to interpret CSF studies...
  15. ncbi request reprint A novel Polish presenilin-1 mutation (P117L) is associated with familial Alzheimer's disease and leads to death as early as the age of 28 years
    T Wisniewski
    Department of Neurology, New York University Medical Center, NY 10016, USA
    Neuroreport 9:217-21. 1998
    ..What role PS has in the pathogenesis of AD remains to be determined, however, the severity of the clinical picture associated with this PS1 mutation stresses the importance of presenilin...
  16. ncbi request reprint The "nonamyloidogenic" p3 fragment (amyloid beta17-42) is a major constituent of Down's syndrome cerebellar preamyloid
    M Lalowski
    Department of Pathology, New York University Medical Center, New York, New York 10016, USA
    J Biol Chem 271:33623-31. 1996
    ..This 26-residue peptide is also present in low quantities in neuritic plaques. We suggest that preamyloid can now be defined biochemically as lesions in which a major Abeta peptide is p3...
  17. pmc Presenilin-1 is associated with Alzheimer's disease amyloid
    T Wisniewski
    Department of Neurology, New York University Medical Center, New York 10016, USA
    Am J Pathol 151:601-10. 1997
    ..It remains to be determined whether all of these proteins are involved in the same or different pathological pathway(s) and which of these proteins is the most important for the common, late-onset form of AD...
  18. ncbi request reprint The prionoses and other conformational disorders
    T Wisniewski
    Department of Neurology, New York University Medical Center, NY 10016, USA
    Amyloid 5:212-24. 1998
    ..Our growing understanding of the mechanisms involved in this category of diseases, raises the possibility of therapeutic approaches based directly on the prevention and reversal of pathologic protein conformation...
  19. ncbi request reprint Alzheimer's presenilin 1 gene expression in platelets and megakaryocytes. Identification of a novel splice variant
    R Vidal
    Department of Pathology, New York University Medical Center, NY 10016, USA
    FEBS Lett 393:19-23. 1996
    ..After RT-PCR we observed that platelets and megakaryocytes carry at least four different PS1 transcripts. One of them is a novel PS1 splice variant that lacks the coding sequence for exon 10 resulting in a shorter 409 amino acid protein...
  20. ncbi request reprint Biology of A beta amyloid in Alzheimer's disease
    T Wisniewski
    Department of Neurology, New York University Medical Center, New York 10016, USA
    Neurobiol Dis 4:313-28. 1997
    ..1996) have the greatest likelihood to make a significant impact on controlling amyloid accumulation in AD...
  21. ncbi request reprint Biochemical and conformational variability of human prion strains in sporadic Creutzfeldt-Jakob disease
    P Aucouturier
    Department of Pathology, New York University School of Medicine, NY 10016, USA
    Neurosci Lett 274:33-6. 1999
    ..Although the average beta-sheet content was higher among type 1 isolates, there was overlap between the two types. Our study suggests that human sporadic CJD-related prions display a significant heterogeneity...
  22. ncbi request reprint Micropreparative gel electrophoresis of low-molecular-weight peptides: purification of highly insoluble amyloid peptide fragments
    M Baumann
    Department of Pathology, New York University Medical Center, New York 10016, USA
    Anal Biochem 236:191-8. 1996
    ..Our results show that micropreparative gel electrophoresis is an effective tool for the isolation of not only larger polypeptides but also small peptide fragments in a form suitable for further biological use...
  23. ncbi request reprint C-terminal fragments of alpha- and beta-tubulin form amyloid fibrils in vitro and associate with amyloid deposits of familial cerebral amyloid angiopathy, British type
    M H Baumann
    Department of Pathology, New York University Medical Center, New York 10016, USA
    Biochem Biophys Res Commun 219:238-42. 1996
    ..These findings suggest that the C-terminal fragments of both alpha- and beta-tubulin are closely associated to the amyloid deposits of familial amyloidosis, British type...
  24. ncbi request reprint Apolipoprotein E isoform-specific regulation of dendritic spine morphology in apolipoprotein E transgenic mice and Alzheimer's disease patients
    Y Ji
    Department of Neurology, New York University School of Medicine, New York, NY 10016, USA
    Neuroscience 122:305-15. 2003
    ..0008) and aged normal controls (P=0.0015). Our findings provide one potential explanation for the increased cognitive decline seen in aged and AD patients expressing apoE4...
  25. pmc The cerebrospinal-fluid soluble form of Alzheimer's amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex
    J Ghiso
    Department of Pathology, New York University Medical Center, NY 10016
    Biochem J 293:27-30. 1993
    ..Immunoprecipitation with anti-SP-40,40 retrieved soluble A beta from cerebrospinal fluid, indicating that the interaction occurs in vivo...
  26. ncbi request reprint Localization of alpha-tocopherol transfer protein in the brains of patients with ataxia with vitamin E deficiency and other oxidative stress related neurodegenerative disorders
    R P Copp
    Department of Medicine, New York University Medical Center, 550 First Avenue, New York, NY 10016, USA
    Brain Res 822:80-7. 1999
    ..We demonstrate the presence of alpha-TTP in cerebellar Purkinje cells in patients having vitamin E deficiency states or diseases associated with oxidative stress...
  27. ncbi request reprint Inhibition of neurite outgrowth by familial Alzheimer's disease-linked presenilin-1 mutations
    W K Dowjat
    Institute for Basic Research in Developmental Disabilities, Staten Island, New York, NY 10314 6399, USA
    Neurosci Lett 267:141-4. 1999
    ....
  28. ncbi request reprint Therapeutic effects of astrocytes expressing both tyrosine hydroxylase and brain-derived neurotrophic factor on a rat model of Parkinson's disease
    Z H Wang
    Department of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA
    Neuroscience 113:629-40. 2002
    ..Our data indicate that the combined use of TH and BDNF has a synergistic therapeutic effect, and is more efficient for the treatment of PD than a single gene therapy using either TH or BDNF alone...
  29. pmc Meningocerebrovascular amyloidosis associated with a novel transthyretin mis-sense mutation at codon 18 (TTRD 18G)
    R Vidal
    Department of Pathology, New York University Medical Center, NY 10016, USA
    Am J Pathol 148:361-6. 1996
    ..With this report we establish that transthyretin amyloid deposition can also produce central nervous system dysfunction as the major clinical symptom...

Research Grants1

  1. Immunization Approaches for Alzheimer's Disease
    Thomas Wisniewski; Fiscal Year: 2007
    ..Lay Summary: AD is the most common cause of dementia. Vaccination is potentially an effective treatment, but is associated with significant toxicity in about 6% of patients. We propose studies to help develop safe, effective vaccines. ..