Long-Term Accumulation of Amyloid-β, β-Secretase, Presenilin-1, and Caspase-3 in Damaged Axons Following Brain Trauma
Top Cited Papers
Open Access
- 1 August 2004
- journal article
- research article
- Published by Elsevier in The American Journal of Pathology
- Vol. 165 (2) , 357-371
- https://doi.org/10.1016/s0002-9440(10)63303-2
Abstract
No abstract availableKeywords
Funding Information
- National Institutes of Health (AG11542, NS38104, NS08803)
This publication has 83 references indexed in Scilit:
- Cell death induced by a caspase-cleaved transmembrane fragment of the Alzheimer amyloid precursor proteinCell Death & Differentiation, 2002
- Axonal Damage in Traumatic Brain InjuryThe Neuroscientist, 2000
- Regulation of APP cleavage by α‐, β‐ and γ‐secretasesFEBS Letters, 2000
- Kinesin and Kinectin Can Associate with the Melanosomal Surface and Form a Link with Microtubules in Normal Human Melanocytes1Journal of Investigative Dermatology, 2000
- Prolonged Activation of NF-κB Following Traumatic Brain Injury in RatsJournal of Neurotrauma, 1999
- Alzheimer's disease after remote head injury: an incidence study.Journal of Neurology, Neurosurgery & Psychiatry, 1997
- Mutant and native human β-amyloid precursor proteins in transgenic mouse brainNeurobiology of Aging, 1995
- Traumatic brain injury in rat produces changes of β-amyloid precursor protein immunoreactivityNeuroReport, 1995
- β-Amyloid precursor protein (βAPP) as a marker for axonal injury after head injuryNeuroscience Letters, 1993
- A molecular dissection of the carboxyterminal tails of the major neurofilament subunits NF‐M and NF‐HJournal of Neuroscience Research, 1991