Memory impairment and cholinergic dysfunction by centrally administered Aβ and carboxyl‐terminal fragment of Alzheimer's APP in mice
- 18 June 2001
- journal article
- Published by Wiley in The FASEB Journal
- Vol. 15 (10) , 1816-1818
- https://doi.org/10.1096/fj.00-0859fje
Abstract
No abstract availableFunding Information
- Ministry of Science and Technology (HMP-98-N-6-0002)
- Ministry of Health and Welfare (HMP-98-N-6-0002)
This publication has 53 references indexed in Scilit:
- Neurotoxic APP C-terminal and β-amyloid domains colocalize in the nuclei of substantia nigra pars reticulata neurons undergoing delayed degenerationBrain Research, 2000
- Increased Activity‐Regulating and Neuroprotective Efficacy of α‐Secretase‐Derived Secreted Amyloid Precursor Protein Conferred by a C‐Terminal Heparin‐Binding DomainJournal of Neurochemistry, 1996
- Secreted Forms of β‐Amyloid Precursor Protein Protect Against Ischemic Brain InjuryJournal of Neurochemistry, 1994
- Administration of amyloid β-peptides into the medial septum of rats decreases acetylcholine release from hippocampus in vivoBrain Research, 1994
- In vivo neurotoxicity of beta-amyloid [β(1–40)] and the β(25–35) fragmentNeurobiology of Aging, 1992
- An in vivo model for the neurodegenerative effects of beta amyloid and protection by substance P.Proceedings of the National Academy of Sciences, 1991
- Neurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin NeuropeptidesScience, 1990
- Is the neuronal basis of Alzheimer's disease cholinergic or glutamatergic?The FASEB Journal, 1990
- Cleavage of Amyloid β Peptide During Constitutive Processing of Its PrecursorScience, 1990
- Senile dementia of the Alzheimer typeAnnals of Neurology, 1983