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- Publications
- Influence
Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles Intracellular Aβ and Synaptic Dysfunction
- S. Oddo, A. Caccamo, +7 authors F. Laferla
- Biology, Medicine
- Neuron
- 31 July 2003
The neuropathological correlates of Alzheimer's disease (AD) include amyloid-beta (Abeta) plaques and neurofibrillary tangles. To study the interaction between Abeta and tau and their effect on… Expand
A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity
- S. Weggen, J. Eriksen, +11 authors E. Koo
- Chemistry, Medicine
- Nature
- 8 November 2001
Epidemiological studies have documented a reduced prevalence of Alzheimer's disease among users of nonsteroidal anti-inflammatory drugs (NSAIDs). It has been proposed that NSAIDs exert their… Expand
An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants.
- N. Suzuki, T. Cheung, +5 authors S. Younkin
- Biology, Medicine
- Science
- 27 May 1994
Normal processing of the amyloid beta protein precursor (beta APP) results in secretion of a soluble 4-kilodalton protein essentially identical to the amyloid beta protein (A beta) that forms… Expand
Production of the Alzheimer amyloid beta protein by normal proteolytic processing.
- M. Shoji, T. Golde, +7 authors B. Frangione
- Biology, Medicine
- Science
- 2 October 1992
The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid… Expand
Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity
- Yong-Jie Zhang, Y. Xu, +14 authors L. Petrucelli
- Biology, Medicine
- Proceedings of the National Academy of Sciences
- 5 May 2009
Inclusions of TAR DNA-binding protein-43 (TDP-43), a nuclear protein that regulates transcription and RNA splicing, are the defining histopathological feature of frontotemporal lobar degeneration… Expand
NSAIDs and enantiomers of flurbiprofen target gamma-secretase and lower Abeta 42 in vivo.
- J. Eriksen, S. Sagi, +8 authors T. Golde
- Medicine
- The Journal of clinical investigation
- 2003
Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development of Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and… Expand
Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice
- E. Mcgowan, Fiona Pickford, +17 authors T. Golde
- Chemistry, Medicine
- Neuron
- 21 July 2005
Considerable circumstantial evidence suggests that Abeta42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis. However, the absolute requirement for Abeta42 for amyloid deposition… Expand
Release of excess amyloid beta protein from a mutant amyloid beta protein precursor.
- X. Cai, T. Golde, S. Younkin
- Biology, Medicine
- Science
- 22 January 1993
The 4-kilodalton amyloid beta protein (A beta), which forms fibrillar deposits in Alzheimer's disease (AD), is derived from a large protein referred to as the amyloid beta protein precursor (beta… Expand
NSAIDs and enantiomers of flurbiprofen target γ-secretase and lower Aβ42 in vivo
- J. Eriksen, S. Sagi, +8 authors T. Golde
- Chemistry
- 1 August 2003
Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development of Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and… Expand
Suppression of hippocampal TRPM7 protein prevents delayed neuronal death in brain ischemia
- H. Sun, M. Jackson, +11 authors M. Tymianski
- Medicine
- Nature Neuroscience
- 1 October 2009
Cardiac arrest victims may experience transient brain hypoperfusion leading to delayed death of hippocampal CA1 neurons and cognitive impairment. We prevented this in adult rats by inhibiting the… Expand
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