Amyloid β protein disruption of cholinergic and growth factor phosphoslipase C signals could underlie cognitive and neurodegerative aspects of Alzheimer's disease
- 31 December 1994
- journal article
- Published by Elsevier in Neurobiology of Aging
- Vol. 15, 95-96
- https://doi.org/10.1016/0197-4580(94)90181-3
Abstract
No abstract availableKeywords
This publication has 18 references indexed in Scilit:
- Cholinergic and serotonergic stimulation of phosphoinositide hydrolysis is decreased in Alzheimer's diseaseLife Sciences, 1994
- β-Amyloid Protein Amplifies Calcium Signaling in Central Neurons from the Adult MouseBiochemical and Biophysical Research Communications, 1993
- Alzheimer's Disease: The Amyloid Cascade HypothesisScience, 1992
- Loss of high‐affinity agonist binding to M1 muscarinic receptors in Alzheimer's disease: Implications for the failure of cholinergic replacement therapiesAnnals of Neurology, 1991
- Phosphatidylinositol-Derived Precursors and SignalsAnnual Review of Cell Biology, 1990
- Decreased levels of protein kinase C in Alzheimer brainBrain Research, 1988
- Long-Term Neuropathological and Neurochemical Effects of Nucleus Basalis Lesions in the RatScience, 1987
- Cholinergic‐ and Adrenergic‐Stimulated Inositide Hydrolysis in Brain: Interaction, Regional Distribution, and Coupling MechanismsJournal of Neurochemistry, 1985
- Alzheimer's Disease: A Disorder of Cortical Cholinergic InnervationScience, 1983
- The Cholinergic Hypothesis of Geriatric Memory DysfunctionScience, 1982