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Amyloid beta peptides, locus coeruleus-norepinephrine system and dense core vesicles
Journal article   Open access   Peer reviewed

Amyloid beta peptides, locus coeruleus-norepinephrine system and dense core vesicles

Jennifer A Ross, Beverly A S Reyes and Elisabeth J Van Bockstaele
Brain research, v 1702, pp 46-53
01 Jan 2019
DOI: https://doi.org/10.1016/j.brainres.2018.03.009
PMID: 29577889
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://europepmc.org/articles/pmc6375485View
Accepted (AM) Open Open Access (License Unspecified)

Abstract

Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Animals Brain - metabolism Cerebral Cortex - metabolism Disease Models, Animal Hippocampus - metabolism Humans Locus Coeruleus - physiology Neurons - metabolism Neuropeptides - metabolism Norepinephrine - metabolism Norepinephrine - physiology Secretory Vesicles - pathology Secretory Vesicles - physiology
The evolution of peptidergic signaling systems in the central nervous system serves a distinct and crucial role in brain processes and function. The diversity of physiological peptides and the complexity of their regulation and secretion from the dense core vesicles (DCV) throughout the brain is a topic greatly in need of investigation, though recent years have shed light on cellular and molecular mechanisms that are summarized in this review. Here, we focus on the convergence of peptidergic systems onto the Locus Coeruleus (LC), the sole provider of norepinephrine (NE) to the cortex and hippocampus, via large DCV. As the LC-NE system is one of the first regions of the brain to undergo degeneration in Alzheimer's Disease (AD), and markers of DCV have consistently been demonstrated to have biomarker potential for AD progression, here we summarize the current literature linking the LC-NE system with DCV dysregulation and Aβ peptides. We also include neuroanatomical data suggesting that the building blocks of senile plaques, Aβ monomers, may be localized to DCV of the LC and noradrenergic axon terminals of the prefrontal cortex. Finally, we explore the putative consequences of chronic stress on Aβ production and the role that DCV may play in LC degeneration. Clinical data of immunological markers of DCV in AD patients are discussed.

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