Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Quantitative neurohistological features of frontotemporal degeneration.
S E Arnold; L Y Han; C M Clark; M Grossman; J Q Trojanowski (Profiled Authors: Trojanowski, John Q; Grossman, Murray)
Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. alveus@mail.med.upenn.edu
Neurobiology of aging 2000;21(6):913-9.
Frontotemporal degeneration (FTD) is a neurodegenerative condition that has been principally associated with frontal lobe dementia. In this study, we compared neuropathological abnormalities in frontal, hippocampal, and calcarine cortices from patients assigned a diagnosis of FTD, normal elderly and Alzheimer's disease (AD). Densities of Nissl-stained neurons and lesions which were immunolabeled for tau, beta-amyloid (Abeta), alpha- and beta-synuclein, ubiquitin, glial fibrillary acidic protein (GFAP) and CD68 antigen were determined using computer-assisted, non-biased quantitative microscopy. We found that FTD frontal and hippocampal regions exhibited marked neuron loss, abundant ubiquitin-immunoreactive (ir) dystrophic neurites, GFAP-ir astrocytes, and CD68-ir microglia, while calcarine cortex was spared. No alpha- or beta-synuclein-ir lesions were observed, and neither the density of tau-ir neurofibrillary tangles nor that of Abeta-ir plaques in FTD exceeded normal controls. In addition, there were no neuropathological differences between FTD subjects who presented clinically with a frontal lobe dementia versus an AD-like dementia. These findings indicate that FTD is a category of neurodegnerative dementias with varying clinical presentations that is characterized by the progressive degeneration of select populations of cortical neurons. The molecular neurodegenerative mechanisms that lead to FTD remain to be elucidated.
2 Originating Grant
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1.
TROJANOWSKI, JOHN Q.
Alzheimer's Disease Core Center
15 July 1997 - 30 June 2016
NATIONAL INSTITUTE ON AGING
Total Funding: $ 25,158,594
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2.
Trojanowski, John Q
Molecular substrates of aging and neuron death
15 May 1997 - 30 April 2010
NATIONAL INSTITUTE ON AGING
Total Funding: $ 24,601,856
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
PRICE, DONALD L
Scavenger Receptors Type-A of Microglia Promote Abeta Uptake After Abeta Immunot
1 December 2009 - 30 November 2012
FOGARTY INTERNATIONAL CENTER
Total Funding: $ 95,865
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2.
MASLIAH, ELIEZER
Clearance Pathways in the CNS in Aging and HIV
1 May 2012 - 30 April 2017
NATIONAL INSTITUTE ON AGING
Total Funding: $ 387,292
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3.
RAPOPORT, STANLEY I
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,242,387
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