C F Lippa

Summary

Publications

  1. pmc Lewy bodies contain altered alpha-synuclein in brains of many familial Alzheimer's disease patients with mutations in presenilin and amyloid precursor protein genes
    C F Lippa
    Department of Neurology, Allegheny University of the Health Sciences MCP Division, Philadelphia, Pennsylvania 19129, USA
    Am J Pathol 153:1365-70. 1998
  2. ncbi request reprint TGF-beta receptors-I and -II immunoexpression in Alzheimer's disease: a comparison with aging and progressive supranuclear palsy
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19129, USA
    Neurobiol Aging 19:527-33. 1998
  3. ncbi request reprint Deposition of beta-amyloid subtypes 40 and 42 differentiates dementia with Lewy bodies from Alzheimer disease
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19129, USA
    Arch Neurol 56:1111-8. 1999
  4. ncbi request reprint AMY plaques in familial AD: comparison with sporadic Alzheimer's disease
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19102, USA
    Neurology 54:100-4. 2000
  5. ncbi request reprint Frontotemporal dementia: report of a familial case
    M Shafiq
    Department of Neurology, MCP-Hahnemann University, Philadelphia, PA, USA
    Neurology 56:S31-4. 2001
  6. ncbi request reprint Alpha-synuclein in familial Alzheimer disease: epitope mapping parallels dementia with Lewy bodies and Parkinson disease
    C F Lippa
    Department of Neurology, Medical College of Pennsylvania Hahnemann University, 3300 Henry Ave, Philadelphia, PA 19129, USA
    Arch Neurol 58:1817-20. 2001
  7. ncbi request reprint Frontotemporal dementia with novel tau pathology and a Glu342Val tau mutation
    C F Lippa
    Department of Neurology, Medical College of Pennsylvania Hahnemann University, Philadelphia 19129, USA
    Ann Neurol 48:850-8. 2000
  8. ncbi request reprint Beta-amyloid, neuronal death and Alzheimer's disease
    J Carter
    Department of Neurology, Medical College of Pennsylvania-Hahnemann University, Philadelphia 19129, USA
    Curr Mol Med 1:733-7. 2001
  9. doi request reprint Disease modifying drugs targeting β-amyloid
    S N Ozudogru
    Department of Neurology, Drexel University College of Medicine, Philadelphia, PA 19102, USA
    Am J Alzheimers Dis Other Demen 27:296-300. 2012
  10. doi request reprint Progranulin (PGRN) expression in ALS: an immunohistochemical study
    D Irwin
    Department of Neurology, Drexel University College of Medicine, Philadelphia, PA 19102, USA
    J Neurol Sci 276:9-13. 2009

Detail Information

Publications10

  1. pmc Lewy bodies contain altered alpha-synuclein in brains of many familial Alzheimer's disease patients with mutations in presenilin and amyloid precursor protein genes
    C F Lippa
    Department of Neurology, Allegheny University of the Health Sciences MCP Division, Philadelphia, Pennsylvania 19129, USA
    Am J Pathol 153:1365-70. 1998
    ..These studies suggest that insoluble alpha-synuclein aggregates into filaments that form LBs in many FAD patients, and we speculate that these inclusions may compromise the function and/or viability of affected neurons in the FAD brain...
  2. ncbi request reprint TGF-beta receptors-I and -II immunoexpression in Alzheimer's disease: a comparison with aging and progressive supranuclear palsy
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19129, USA
    Neurobiol Aging 19:527-33. 1998
    ..We conclude that TGF-beta RI and II immunoreactivity is increased in reactive glia in AD and progressive supranuclear palsy, and RI immunoreactivity may occasionally be increased in neurons in cases with advanced AD...
  3. ncbi request reprint Deposition of beta-amyloid subtypes 40 and 42 differentiates dementia with Lewy bodies from Alzheimer disease
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19129, USA
    Arch Neurol 56:1111-8. 1999
    ..The plaque subtype Abeta(x-42) occurs as an early event, with Abeta(x-40) plaques forming at a later stage. In dementia with Lewy bodies (DLB), an increase in the amount of cortical Abeta occurs without severe cortical neuronal losses...
  4. ncbi request reprint AMY plaques in familial AD: comparison with sporadic Alzheimer's disease
    C F Lippa
    Department of Neurology, MCP Hahnemann University, Philadelphia, PA 19102, USA
    Neurology 54:100-4. 2000
    ..To assess AMY expression in familial AD (FAD)...
  5. ncbi request reprint Frontotemporal dementia: report of a familial case
    M Shafiq
    Department of Neurology, MCP-Hahnemann University, Philadelphia, PA, USA
    Neurology 56:S31-4. 2001
    ..Tau-positive glial cells were also present. The authors suggest that the abnormal tau aggregates are related to the symptoms experienced by affected members of this family...
  6. ncbi request reprint Alpha-synuclein in familial Alzheimer disease: epitope mapping parallels dementia with Lewy bodies and Parkinson disease
    C F Lippa
    Department of Neurology, Medical College of Pennsylvania Hahnemann University, 3300 Henry Ave, Philadelphia, PA 19129, USA
    Arch Neurol 58:1817-20. 2001
    ..However, epitope mapping for alpha-synuclein is distinctive in different neurodegenerative diseases. The reasons for this are poorly understood but may reflect fundamental differences in disease mechanisms...
  7. ncbi request reprint Frontotemporal dementia with novel tau pathology and a Glu342Val tau mutation
    C F Lippa
    Department of Neurology, Medical College of Pennsylvania Hahnemann University, Philadelphia 19129, USA
    Ann Neurol 48:850-8. 2000
    ....
  8. ncbi request reprint Beta-amyloid, neuronal death and Alzheimer's disease
    J Carter
    Department of Neurology, Medical College of Pennsylvania-Hahnemann University, Philadelphia 19129, USA
    Curr Mol Med 1:733-7. 2001
    ..A more general problem with protein processing, damage due to the neuron from accumulation of intraneuronal Abeta or extracellular, preplaque Abeta may also be important as underlying factors in the dementia of AD...
  9. doi request reprint Disease modifying drugs targeting β-amyloid
    S N Ozudogru
    Department of Neurology, Drexel University College of Medicine, Philadelphia, PA 19102, USA
    Am J Alzheimers Dis Other Demen 27:296-300. 2012
    ..Since amyloid is the peptide most closely linked to disease pathogenesis, it is possible that some of the anti-amyloid agents will impact the disease progression in a meaningful way...
  10. doi request reprint Progranulin (PGRN) expression in ALS: an immunohistochemical study
    D Irwin
    Department of Neurology, Drexel University College of Medicine, Philadelphia, PA 19102, USA
    J Neurol Sci 276:9-13. 2009
    ..The meaning of this association is unclear, but may indicate a potential role for PGRN in the variable expression of motor and cognitive deficits in the ALS-FTD spectrum...