[roflmyeggo]

Yet another reason to get a good nights sleep.

Many of these metabolic degradation products (not just beta-amyloid) of neuronal cell activities should readily be cleared quickly and efficiently from the interstitial space of the brain due to the highly sensitive nature of neuronal cells to their environment.

Some negative effects documented from these byproducts include: negatively effecting synaptic transmission[1], decreasing cytosolic Ca2+ concentrations[2] (Ca2+ is one of the final players in the triggering the release of neurotransmitters into the synapse between neurons to facilitate messages), and irreversible neuronal injury[3].

[1] - K. Parameshwaran, M. Dhanasekaran, V. Suppiramaniam, Amyloid beta peptides and glutamatergic synaptic dysregulation. Exp. Neurol. 210, 7–13 (2008)

[2] - K. V. Kuchibhotla, S. T. Goldman, C. R. Lattarulo, H. Y. Wu, B. T. Hyman, B. J. Bacskai, Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks. Neuron 59, 214–225 (2008)

[3] - M. P. Mattson, Calcium and neuronal injury in Alzheimer’s disease. Contributions of beta-amyloid precursor protein mismetabolism, free radicals, and metabolic compromise. Ann. N. Y. Acad. Sci. 747, 50–76 (1994)