By Talia Ogliore, Office of the UH Mānoa Vice Chancellor for Research

A research team at the University of Hawai‘i at Mānoa’s John A. Burns School of Medicine has published new research that highlights the potential role of specific target receptors on nerve cells for β-amyloid toxicity in the earliest stages of Alzheimer’s disease. A major indicator of Alzheimer’s disease is the accumulation in brain tissue of a small, toxic peptide, known as β-amyloid (Aβ), in the form of dense deposits referred to as plaques. However, the levels of Aβ have been found to rise sharply as much as 10 years before a person is diagnosed with the disease. The University of Hawai‘i study focused on key target receptors found on certain nerve cells in brain, which appear to be particularly sensitive to Aβ. These target receptors, normally activated by the neurotransmitter acetylcholine, appear to render these nerve cells highly vulnerable to accumulating Aβ, ultimately triggering their death.

“This study is the first of its kind to use a very tightly defined nerve cell system to attempt to better understand the impact of sustained exposure of Aβ on the regulation of cellular and synaptic function,” said Dr. Robert A. Nichols, UH Mānoa Professor of Cell and Molecular Biology and the principal investigator for this study. The results were published in the April 19, 2013 issue of The Journal of Biological Chemistry.

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Citation:

Arora, K. Alfulaij, N., Higa, J.K., Panee, J., Nichols, R.A. (2013) Impact of Sustained Exposure to β-amyloid on Calcium Homeostasis and Neuronal Integrity in Model Nerve Cell System Expressing α4β2 Nicotinic Acetylcholine Receptors. J. Biol. Chem. 288, 11175-11190