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Genomes and Genes | J Q TrojanowskiSummaryAffiliation: University of Pennsylvania Country: USA Publications
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Enhanced neurofibrillary tangle formation, cerebral atrophy, and cognitive deficits induced by repetitive mild brain injury in a transgenic tauopathy mouse modelYasumasa Yoshiyama
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA
J Neurotrauma 22:1134-41. 2005..The reasons for the augmentation of tau pathologies in only one T44 tau Tg mouse subjected to mrTBI remain to be elucidated...
A model for improving the treatment and care of Alzheimer's disease patients through interdisciplinary researchJohn Q Trojanowski
Institute on Aging, University of Pennsylvania, Philadelphia, PA, USA
Alzheimers Dement 8:564-73. 2012..The "Ware-UPenn" program has been presented in this report as a useful prototype for partnerships between private philanthropy and academia in planning and developing programs to address a major national public health problem...
Phosphorylated tau/amyloid beta 1-42 ratio in ventricular cerebrospinal fluid reflects outcome in idiopathic normal pressure hydrocephalusSunil Patel
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Fluids Barriers CNS 9:7. 2012..abstract:..
Acetylated tau, a novel pathological signature in Alzheimer's disease and other tauopathiesDavid J Irwin
Centre for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Alzheimer s Disease Core Centre, Institute on Ageing, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 6021, USA
Brain 135:807-18. 2012..Thus, inhibiting tau acetylation could be a disease-modifying target for drug discovery target in tauopathies...
Parkinson's disease and related alpha-synucleinopathies are brain amyloidosesJohn Q Trojanowski
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Ann N Y Acad Sci 991:107-10. 2003..Thus, PD and related synucleinopathies are brain amyloidoses that may share similar mechanisms and targets for drug discovery...
PENN neurodegenerative disease research - in the spirit of Benjamin FranklinJohn Q Trojanowski
Institute on Aging, Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Neurosignals 16:5-10. 2008..This research could enhance our chances of aging successfully in the continuing longevity revolution, and the essay here provides context and background on this research...
Proposed neuropathological criteria for the post mortem diagnosis of multiple system atrophyJ Q Trojanowski
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Ageing of the University of Pennsylvania, Philadelphia, PA 19104 4283, USA
Neuropathol Appl Neurobiol 33:615-20. 2007..The deliberations and recommendations of the Working Group on Diagnostic Neuropathology Criteria for MSA are summarized in this report...
Meeting summary--cell biology of Parkinson's disease and related neurodegenerative disordersJohn Q Trojanowski
Center for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Sci Aging Knowledge Environ 2003:PE23. 2003....
"Fatal attractions" of proteins. A comprehensive hypothetical mechanism underlying Alzheimer's disease and other neurodegenerative disordersJ Q Trojanowski
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, HUP, Maloney Building, 3rd Floor, Philadelphia, Pennsylvania 19104 4283, USA
Ann N Y Acad Sci 924:62-7. 2000....
Rous-Whipple Award Lecture. The Alzheimer's brain: finding out what's broken tells us how to fix itJohn Q Trojanowski
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Maloney 3, HUP, 3600 Spruce St, Philadelphia, PA 19104-4283, USA
Am J Pathol 167:1183-8. 2005
Transgenic models of tauopathies and synucleinopathiesJ Q Trojanowski
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, The University of Pennsylvania School of Medicine, Philadelphia 19104 4283, USA
Brain Pathol 9:733-9. 1999....
The art and science of anti-aging therapiesJohn Q Trojanowski
Institute on Aging and the Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Sci Aging Knowledge Environ 2005:pe11. 2005..The program, which combined medical, surgical, and nonpharmacological approaches to healthy successful aging, gave attendees the opportunity to make sense of the issues at hand and to sort out safe treatments from perilous quick fixes...
Living Longer and Paying the Price?John Q Trojanowski
The Institute on Aging, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Sci Aging Knowledge Environ 2005:pe38. 2005..Further, speakers presented their views on covering the costs of public and private programs for future generations of older adults...
The role of tau in Alzheimer's diseaseJohn Q Trojanowski
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Maloney Building, 3rd Floor, HUP, Philadelphia, PA 19104, USA
Med Clin North Am 86:615-27. 2002....
"Emerging Alzheimer's disease therapies: focusing on the future"John Q Trojanowski
Department of Pathology and Laboratory Medicine, The Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia 19104 4283, USA
Neurobiol Aging 23:985-90. 2002..The symposium is summarized here followed by reviews from symposium speakers who describe potential anti-Abeta therapies some of which are in clinical trials...
Neocortical and hippocampal amyloid-β and tau measures associate with dementia in the oldest-oldJohn L Robinson
Center for Neurodegenerative Disease Research, Institute on Ageing, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Brain 134:3708-15. 2011....
Neuropathological verisimilitude in animal models of Alzheimer's disease: key to elucidating neurodegenerative pathways and identifying new targets for drug discoveryJohn Q Trojanowski
Department of Pathology and Laboratory Medicine, Division of Anatomical Pathology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA
Am J Pathol 160:409-11. 2002
Novel CSF biomarkers for frontotemporal lobar degenerationsW T Hu
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104 4283, USA
Neurology 75:2079-86. 2010..To identify antemortem CSF diagnostic biomarkers that can potentially distinguish between the 2 main causes of frontotemporal lobar degeneration (FTLD), i.e., FTLD with TDP-43 pathology (FTLD-TDP) and FTLD with tau pathology (FTLD-tau)...
Protein mis-folding emerges as a "drugable" target for discovery of novel therapies for neuropsychiatric diseases of agingJohn Q Trojanowski
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Am J Geriatr Psychiatry 12:134-5. 2004
Update on the biomarker core of the Alzheimer's Disease Neuroimaging Initiative subjectsJohn Q Trojanowski
Department of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Alzheimers Dement 6:230-8. 2010..Further studies in ADNI will refine this model and render the biomarkers studied in ADNI more applicable to routine diagnosis and to clinical trials of disease modifying therapies...
Design of comprehensive Alzheimer's disease centers to address unmet national needsJohn Q Trojanowski
Institute on Aging, Philadelphia, PA, USA
Alzheimers Dement 6:150-5. 2010..The intent of this position paper is to stimulate thinking and foster the development of other or alternative models for a systematic approach to the study of dementia and movement disorders...
New directions for frontotemporal dementia drug discoveryJohn Q Trojanowski
Institute on Aging, Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Alzheimers Dement 4:89-93. 2008..The recognition that almost all forms of FTD are due to TDP-43 proteinopathies and tauopathies creates new opportunities for FTD drug discovery targeting pathways of TDP-43 and tau-mediated neurodegeneration...
Overview of protein aggregation in single, double, and triple neurodegenerative brain amyloidosesJohn Q Trojanowski
Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Neuromolecular Med 4:1-6. 2003
Parkinson's disease and related synucleinopathies are a new class of nervous system amyloidosesJohn Q Trojanowski
Department of Pathology, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
Neurotoxicology 23:457-60. 2002..Continuing advances in this research direction should advance understanding of PD and accelerate discovery of more effective therapies for this and related synucleinopathies...
Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesionsB I Giasson
Center for Neurodegenerative Disease Research and Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Science 290:985-9. 2000..The selective and specific nitration of alpha-synuclein in these disorders provides evidence to directly link oxidative and nitrative damage to the onset and progression of neurodegenerative synucleinopathies...
Radioiodinated styrylbenzenes and thioflavins as probes for amyloid aggregatesZ P Zhuang
Departments of Radiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Med Chem 44:1905-14. 2001....
Brain trauma induces massive hippocampal neuron death linked to a surge in beta-amyloid levels in mice overexpressing mutant amyloid precursor proteinD H Smith
Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104 6316, USA
Am J Pathol 153:1005-10. 1998..01). These data suggest a mechanistic link between brain trauma and Abeta levels and the death of neurons...
Attenuated neurodegenerative disease phenotype in tau transgenic mouse lacking neurofilamentsT Ishihara
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Neurosci 21:6026-35. 2001....
Absence of neurodegeneration and neural injury in the cerebral cortex in a sample of elderly patients with schizophreniaS E Arnold
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
Arch Gen Psychiatry 55:225-32. 1998..However, we hypothesized that relatively small accumulations of age- or disease-related neurodegenerative lesions occurring in an otherwise abnormal brain could result in deterioration in schizophrenia...
Glial cytoplasmic inclusions in white matter oligodendrocytes of multiple system atrophy brains contain insoluble alpha-synucleinP H Tu
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, USA
Ann Neurol 44:415-22. 1998....
Autosomal dominant dementia with widespread neurofibrillary tanglesL A Reed
Department of Pathology, University of Iowa Hospitals and Clinics, Iowa City 52242, USA
Ann Neurol 42:564-72. 1997....
Factors associated with survival probability in autopsy-proven frontotemporal lobar degenerationS X Xie
Department of Biostatistics and Epidemiology, University of Pennsylvania School of Medicine Philadelphia, PA, USA
J Neurol Neurosurg Psychiatry 79:126-9. 2008..To examine the clinical and pathological factors associated with survival in autopsy-confirmed frontotemporal lobar degeneration (FTLD)...
Isomerization of (Z,Z) to (E,E)1-bromo-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene in strong base: probes for amyloid plaques in the brainC W Lee
Department of Radiology, University of Pennsylvania, 3700 Market Street, Room 305, Philadelphia, Pennsylvania 19104, USA
J Med Chem 44:2270-5. 2001..Such information could be exploited to develop new ligands for detecting amyloid plaques in AD...
CSF amyloid {beta} 1-42 predicts cognitive decline in Parkinson diseaseA Siderowf
Department of Neurology, 330 South 9th Street, Second Floor, Philadelphia, PA 19107, USA
Neurology 75:1055-61. 2010..Cognitive decline associated with Parkinson disease (PD) is common and highly disabling. Biomarkers that help identify patients at risk for cognitive decline would be useful additions to the clinical management of the disease...
Tau isoform profile and phosphorylation state in dementia pugilistica recapitulate Alzheimer's diseaseM L Schmidt
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104-4283, USA
Acta Neuropathol 101:518-24. 2001....
Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injuryValeria Conte
Head Injury Center, University of Pennsylvania, Philadelphia, Pennsylvania, USA
J Neurochem 90:758-64. 2004..This study suggests that the exacerbation of brain oxidative stress following RCBI plays a mechanistic role in accelerating Alphabeta accumulation and behavioral impairments in the Tg2576 mice...
Repetitive mild brain trauma accelerates Abeta deposition, lipid peroxidation, and cognitive impairment in a transgenic mouse model of Alzheimer amyloidosisKunihiro Uryu
Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4283, USA
J Neurosci 22:446-54. 2002....
Retarded axonal transport of R406W mutant tau in transgenic mice with a neurodegenerative tauopathyBin Zhang
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4283, USA
J Neurosci 24:4657-67. 2004....
Frontotemporal dementia progresses to death faster than Alzheimer diseaseE D Roberson
Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA
Neurology 65:719-25. 2005..Frontotemporal lobar degeneration (FTLD) is a common cause of non-Alzheimer dementia, but its natural history and the factors related to mortality in affected patients are not well understood...
A panel of epitope-specific antibodies detects protein domains distributed throughout human alpha-synuclein in Lewy bodies of Parkinson's diseaseB I Giasson
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104 4283, USA
J Neurosci Res 59:528-33. 2000....
Prominent perikaryal expression of alpha- and beta-synuclein in neurons of dorsal root ganglion and in medullary neuronsB I Giasson
Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Exp Neurol 172:354-62. 2001....
Spinal cord neurofibrillary pathology in Alzheimer disease and Guam Parkinsonism-dementia complexM L Schmidt
Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia 19104-4283, USA
J Neuropathol Exp Neurol 60:1075-86. 2001..Western blot analysis confirmed this by revealing that sarcosyl insoluble tau in spinal cord extracts from patients with NFTs exhibited the presence of all 6 tau isoforms similar to that from AD and ALS/PDC cortical gray matter...
Longitudinal decline in autopsy-defined frontotemporal lobar degenerationM Grossman
Department of Neurology, University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104 4283, USA
Neurology 70:2036-45. 2008..The natural history of patients with pathologically proven frontotemporal lobar degeneration (FTLD) is important from clinical and biologic perspectives, but is not well documented quantitatively...
Quantitative neurohistological features of frontotemporal degenerationS E Arnold
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Neurobiol Aging 21:913-9. 2000..The molecular neurodegenerative mechanisms that lead to FTD remain to be elucidated...
Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosisManuela Neumann
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Science 314:130-3. 2006..TDP-43 represents the common pathologic substrate linking these neurodegenerative disorders...
Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson's diseasePavan K Auluck
Department of Neuroscience, University of Pennsylvania and University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Science 295:865-8. 2002..Furthermore, Lewy bodies in human postmortem tissue immunostained for molecular chaperones, also suggesting that chaperones may play a role in Parkinson's disease progression...
BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivoEdward B Lee
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine
J Cell Biol 168:291-302. 2005....
Initiation and synergistic fibrillization of tau and alpha-synucleinBenoit I Giasson
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine
Science 300:636-40. 2003..This suggests that interactions between alpha-syn and tau can promote their fibrillization and drive the formation of pathological inclusions in human neurodegenerative diseases...
Neurodegeneration with brain iron accumulation, type 1 is characterized by alpha-, beta-, and gamma-synuclein neuropathologyJ E Galvin
Department of Neurology, Medical College of Pennsylvania Hahnemann University the Center for Neurodegenerative Disease Research, and the Department of Neurology, The University of Pennsylvania, Philadelphia, Pennsylvania, USA
Am J Pathol 157:361-8. 2000..These findings expand the concept of neurodegenerative synucleinopathies by implicating alphaS, betaS, and gammaS in the pathogenesis of NBIA 1...
Abnormal tau phosphorylation at Ser396 in Alzheimer's disease recapitulates development and contributes to reduced microtubule bindingG T Bramblett
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104 4283
Neuron 10:1089-99. 1993..Thus, phosphorylation of Ser396 may destabilize MTs in AD, resulting in the degeneration of affected cells...
Age-dependent synuclein pathology following traumatic brain injury in miceK Uryu
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Exp Neurol 184:214-24. 2003..This model of age-dependent TBI-induced transient alterations in alpha-Syn provides an opportunity to examine possible links between TBI and mechanisms of disease in synucleinopathies...
Age-dependent induction of congophilic neurofibrillary tau inclusions in tau transgenic miceT Ishihara
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Am J Pathol 158:555-62. 2001....
Axon pathology in Parkinson's disease and Lewy body dementia hippocampus contains alpha-, beta-, and gamma-synucleinJ E Galvin
Department of Neurology, Medical College of Pennsylvania, Hahnemann University, 245 North 15th Street, Philadelphia, PA 19129, USA
Proc Natl Acad Sci U S A 96:13450-5. 1999..Our findings broaden the concept of neurodegenerative "synucleinopathies" by implicating betaS and gammaS, in addition to alphaS, in the onset/progression of PD and DLB...
Cognitive and motor assessment in autopsy-proven corticobasal degenerationR Murray
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Neurology 68:1274-83. 2007..To investigate the clinical features of autopsy-proven corticobasal degeneration (CBD)...
Cortical biochemistry in MCI and Alzheimer disease: lack of correlation with clinical diagnosisM S Forman
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 422 Curie Blvd, 605B Stellar Chance Building, Philadelphia, PA 19104, USA
Neurology 68:757-63. 2007..Mild cognitive impairment, hypothesized to be prodromal Alzheimer disease (AD), shows abundant senile plaques and neurofibrillary tangles, but its biochemical correlates remain undefined...
Loss of brain tau defines novel sporadic and familial tauopathies with frontotemporal dementiaV Zhukareva
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
Ann Neurol 49:165-75. 2001..The presence of tau mRNA in these brains suggests that the level of tau protein may be controlled posttranscriptionally, at the level of either translation or mRNA stability...
Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson's diseaseH I Hurtig
Department of Neurology, University of Pennsylvania, PA, USA
Neurology 54:1916-21. 2000..Although Alzheimer's pathology has been a frequent finding, recent advances in immunostaining of alpha-synuclein have suggested the possible importance of cortical Lewy bodies (CLBs) in the brains of demented patients with PD...
AMY plaques in familial AD: comparison with sporadic Alzheimer's diseaseC 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)...
Cerebrospinal fluid profile in frontotemporal dementia and Alzheimer's diseaseMurray Grossman
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Ann Neurol 57:721-9. 2005..We conclude that CSF tau levels are significantly reduced in many patients with FTD...
Early vitamin E supplementation in young but not aged mice reduces Abeta levels and amyloid deposition in a transgenic model of Alzheimer's diseaseSyuan Sung
Center for Experimental Therapeutics, Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
FASEB J 18:323-5. 2004..These results support the hypothesis that oxidative stress is an important early event in AD pathogenesis, and antioxidant therapy may be beneficial only if given at this stage of the disease process...
Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synucleinBenoit I Giasson
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, 3600 Spruce Street, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
Neuron 34:521-33. 2002..These mice demonstrate that A53T alpha-synuclein leads to the formation of toxic filamentous alpha-synuclein neuronal inclusions that cause neurodegeneration...
Glial fibrillary acidic protein-immunoreactive astrocytosis in elderly patients with schizophrenia and dementiaS E Arnold
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
Acta Neuropathol 91:269-77. 1996..In the absence of any diagnostic neuropathological findings in this subgroup, the implications of these observations for the pathogenesis of schizophrenia remain to be determined...
Frontotemporal dementia: report of a familial caseM 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...
Early fetal acquisition of the chromaffin and neuronal immunophenotype by human adrenal medullary cells. An immunohistological study using monoclonal antibodies to chromogranin A, synaptophysin, tyrosine hydroxylase, and neuronal cytoskeletal proteinsW M Molenaar
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104
Exp Neurol 108:1-9. 1990..They suggest that "large" and "small" cells are progenitors of the chromaffin and the ganglion cells, respectively, of the mature adrenal medulla...
Multimodal predictors for Alzheimer disease in nonfluent primary progressive aphasiaW T Hu
Department of Neurology, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, PA 19106, USA
Neurology 75:595-602. 2010..We sought to determine the value of clinical characterization, neuropsychological analysis, and MRI atrophy in predicting pathology of LPA and PNFA...
Impaired glutamate transport in a mouse model of tau pathology in astrocytesDeepa V Dabir
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Children s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Neurosci 26:644-54. 2006..Thus, these Tg mice recapitulate features of astrocytic pathology observed in tauopathies and implicate a role for altered astrocyte function in the pathogenesis of these disorders...
Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse modelYasumasa Yoshiyama
The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Neuron 53:337-51. 2007..Thus, hippocampal synaptic pathology and microgliosis may be the earliest manifestations of neurodegenerative tauopathies, and abrogation of tau-induced microglial activation could retard progression of these disorders...
Evidence of multisystem disorder in whole-brain map of pathological TDP-43 in amyotrophic lateral sclerosisFelix Geser
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Alzheimer s Disease Core Center, Institute on Aging, Philadelphia, USA
Arch Neurol 65:636-41. 2008....
Mutant and wild type human alpha-synucleins assemble into elongated filaments with distinct morphologies in vitroB I Giasson
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Biol Chem 274:7619-22. 1999....
Clinical and neuropathologic variation in neuronal intermediate filament inclusion diseaseN J Cairns
Center for Neurodegenerative Disease Research, Department University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Neurology 63:1376-84. 2004..Recently described neuronal intermediate filament inclusion disease (NIFID) shows considerable clinical heterogeneity...
Transgenic mouse models of tauopathies: prospects for animal models of Pick's diseaseV M Lee
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, The University of Pennsylvania School of Medicine, Philadelphia, USA
Neurology 56:S26-30. 2001....
The fluorescent Congo red derivative, (trans, trans)-1-bromo-2,5-bis-(3-hydroxycarbonyl-4-hydroxy)styrylbenzene (BSB), labels diverse beta-pleated sheet structures in postmortem human neurodegenerative disease brainsM L Schmidt
Department of Pathology, University of Pennsylvania, Philadelphia 19104-4283, USA
Am J Pathol 159:937-43. 2001....
Frontotemporal dementia with novel tau pathology and a Glu342Val tau mutationC F Lippa
Department of Neurology, Medical College of Pennsylvania Hahnemann University, Philadelphia 19129, USA
Ann Neurol 48:850-8. 2000....
Human fetal hippocampal development: II. The neuronal cytoskeletonS E Arnold
Department of Psychiatry and Neurology, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
J Comp Neurol 367:293-307. 1996..These observations have implications for understanding the role of the neuronal cytoskeleton in the developing, mature, and diseased CNS...
Alpha-synuclein in familial Alzheimer disease: epitope mapping parallels dementia with Lewy bodies and Parkinson diseaseC 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...
Frontotemporal dementia: clinicopathological correlationsMark S Forman
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA
Ann Neurol 59:952-62. 2006....
Alzheimer's disease neuroimaging initiative: a one-year follow up study using tensor-based morphometry correlating degenerative rates, biomarkers and cognitionAlex D Leow
Laboratory of Neuro Imaging, Department of Neurology, UCLA School of Medicine, Los Angeles, CA 90095 1769, USA
Neuroimage 45:645-55. 2009....
Clinical and pathological continuum of multisystem TDP-43 proteinopathiesFelix Geser
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Arch Neurol 66:180-9. 2009....
Nitration of tau protein is linked to neurodegeneration in tauopathiesTakashi Horiguchi
Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Am J Pathol 163:1021-31. 2003..Taken together, these findings imply that nitrative injury is directly linked to the formation of filamentous tau inclusions...
Overexpression of the human NFM subunit in transgenic mice modifies the level of endogenous NFL and the phosphorylation state of NFH subunitsP H Tu
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104 4283, USA
J Cell Biol 129:1629-40. 1995..NFM and NFH proteins may assume similar functions in regulation of NF packing density in vivo...
Second consensus statement on the diagnosis of multiple system atrophyS Gilman
Department of Neurology, University of Michigan, 300 N Ingalls St, 3D15, Ann Arbor, MI 48109 5489, USA
Neurology 71:670-6. 2008..Since then, clinical, laboratory, neuropathologic, and imaging studies have advanced the field, requiring a fresh evaluation of diagnostic criteria. We held a second consensus conference in 2007 and present the results here...
Selective degeneration fo Purkinje cells with Lewy body-like inclusions in aged NFHLACZ transgenic miceP H Tu
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
J Neurosci 17:1064-74. 1997....
RNA sequestration to pathological lesions of neurodegenerative diseasesS D Ginsberg
Center for Neurodegenerative Disease Research and Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104 4283, USA
Acta Neuropathol 96:487-94. 1998..These observations demonstrate the selective localization of RNA species to distinct pathological lesions of neurodegenerative disease brains...
Clinical and pathological diagnosis of frontotemporal dementia: report of the Work Group on Frontotemporal Dementia and Pick's DiseaseG M McKhann
Department of Neurology, Zanvyl Krieger Mind Brain Institute, Johns Hopkins University School of Medicine, 338 Krieger Hall, 3400 N Charles St, Baltimore, MD 21218 2685, USA
Arch Neurol 58:1803-9. 2001..In addition, recommendations for the neuropathological criteria of FTD were reviewed, relative to classical neuropathology and modern molecular biology...
Enhanced brain levels of 8,12-iso-iPF2alpha-VI differentiate AD from frontotemporal dementiaY Yao
Center for Experimental Therapeutics, Department of Pharmacology, University of Pennsylvania, School of Medicine, Philadelphia 19104, USA
Neurology 61:475-8. 2003..The generation of 8,12-iso-iPF(2alpha)-VI in the brain is not a general or final common pathway of neurodegeneration, but may be relatively specific for disease processes in AD and not FTD...
Mild head injury increasing the brain's vulnerability to a second concussive impactH L Laurer
The Head Injury Center, Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104-6316, USA
J Neurosurg 95:859-70. 2001..CONCLUSIONS: On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma...
Corticobasal syndrome and primary progressive aphasia as manifestations of LRRK2 gene mutationsA S Chen-Plotkin
Center for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine, University of Pennsylvania Health System, Philadelphia, PA 19104, USA
Neurology 70:521-7. 2008..Despite pleomorphic pathology, LRRK2 mutations are believed to manifest clinically as typical Parkinson disease (PD). However, most genetic screens have been limited to PD clinic populations...
TDP-43 pathology occurs infrequently in multiple system atrophyF Geser
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Neuropathol Appl Neurobiol 37:358-65. 2011..Consequently, we examined MSA for evidence of TDP-43 or FUS pathology utilizing immunohistochemical studies in autopsy material from 29 MSA patients...
A review and rationale for the use of genetically engineered animals in the study of traumatic brain injuryL Longhi
Department of Neurosurgery, University of Pennsylvania and Veterans Administration Medical Center, Philadelphia, Pennsylvania 19104, USA
J Cereb Blood Flow Metab 21:1241-58. 2001....
PP2A mRNA expression is quantitatively decreased in Alzheimer's disease hippocampusV Vogelsberg-Ragaglia
Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Exp Neurol 168:402-12. 2001..This could result in decreased protein expression and phosphatase activity, leading to the hyperphosphorylation of tau and the formation of NFTs, as well as neuron degeneration in AD...
Lewy bodies contain altered alpha-synuclein in brains of many familial Alzheimer's disease patients with mutations in presenilin and amyloid precursor protein genesC 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...
Alzheimer's pathology in human temporal cortex surgically excised after severe brain injuryMilos D Ikonomovic
Department of Neurology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA
Exp Neurol 190:192-203. 2004....
Amyotrophic lateral sclerosis-plus syndrome with TAR DNA-binding protein-43 pathologyLeo F McCluskey
Department of Neurology, University of Pennsylvania School of Medicine, 330 S 9th St, Philadelphia, PA 19107, USA
Arch Neurol 66:121-4. 2009....
Long-term accumulation of amyloid-beta, beta-secretase, presenilin-1, and caspase-3 in damaged axons following brain traumaXiao-Han Chen
Department of Neurosurgery, University of Pennsylvania, 105C Hayden Hall, 3320 SmithWalk, Philadelphia, PA 19104-6316, USA
Am J Pathol 165:357-71. 2004..The abnormal concentration of these factors may lead to APP proteolysis and Abeta formation within the axonal membrane compartment...
Novel CSF biomarkers for Alzheimer's disease and mild cognitive impairmentWilliam T Hu
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
Acta Neuropathol 119:669-78. 2010..In summary, our targeted proteomic screen revealed novel CSF biomarkers that can improve the distinction between AD and non-AD cases by established biomarkers alone...
Forebrain overexpression of alpha-synuclein leads to early postnatal hippocampal neuron loss and synaptic disruptionYoungshin Lim
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Exp Neurol 221:86-97. 2010..These data imply that developing neurons are more vulnerable to degenerate than mature neurons as a consequence of forebrain WT and mutant alpha-syn overexpression...
Novel method to quantify neuropil threads in brains from elders with or without cognitive impairmentT W Mitchell
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Histochem Cytochem 48:1627-38. 2000..On the basis of data presented here using this novel strategy, we conclude that this quantitative imaging technique will facilitate efforts to determine the behavioral correlations of neuritic lesions in AD and other brain disorders...
The expression of alpha-, beta-, and gamma-synucleins in olfactory mucosa from patients with and without neurodegenerative diseasesJ E Duda
Department of Pathology and Laboratory Medicine, The Center for Neurodegenerative Disease Research, Philadelphia, Pennsylvania, USA
Exp Neurol 160:515-22. 1999..Thus, our data on synuclein expression within the OE may signify that synuclein plays a role in the regeneration and plasticity of ORNs in the adult human OE...
Mild traumatic brain injury induces apoptotic cell death in the cortex that is preceded by decreases in cellular Bcl-2 immunoreactivityR Raghupathi
Department of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
Neuroscience 110:605-16. 2002....
Induction of alpha-synuclein aggregation by intracellular nitrative insultE Paxinou
Stokes Research Institute and Department of Biochemistry and Biophysics, Children's Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Neurosci 21:8053-61. 2001..Our data indicate that nitrative and oxidative insult may initiate pathogenesis of alpha-synuclein aggregates...
TARDBP mutations in amyotrophic lateral sclerosis with TDP-43 neuropathology: a genetic and histopathological analysisVivianna M Van Deerlin
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
Lancet Neurol 7:409-16. 2008..Our aim was to investigate whether TARDBP is a candidate disease gene for familial ALS that is not associated with mutations in superoxide dismutase 1 (SOD1)...
Research Grants
- Alzheimer's Disease Core CenterJohn Trojanowski; Fiscal Year: 2007..abstract_text> ..
