TY - JOUR
T1 - Neuronally derived extracellular vesicles
T2 - An emerging tool for understanding Alzheimer's disease
AU - Watson, Luke S.
AU - Hamlett, Eric D.
AU - Stone, Tyler D.
AU - Sims-Robinson, Catrina
N1 - Publisher Copyright:
© 2019 The Author(s).
PY - 2019/6/10
Y1 - 2019/6/10
N2 - In order for Alzheimer's disease (AD) to manifest, cells must communicate "pathogenic material" such as proteins, signaling molecules, or genetic material to ensue disease propagation. Small extracellular vesicles are produced via the endocytic pathways and released by nearly all cell types, including neurons. Due to their intrinsic interrelationship with endocytic processes and autophagy, there has been increased interest in studying the role of these neuronally-derived extracellular vesicles (NDEVs) in the propagation of AD. Pathologic cargo associated with AD have been found in a number of studies, and NDEVs have been shown to induce pathogenesis in vivo and in vitro. Exogenous NDEVs are also shown to reduce plaque burden in AD models. Thus, the NDEV has the potential to become a useful biomarker, a pathologic potentiator, and a therapeutic opportunity. While the field of NDEV research in AD is still in its infancy, we review the current literature supporting these three claims.
AB - In order for Alzheimer's disease (AD) to manifest, cells must communicate "pathogenic material" such as proteins, signaling molecules, or genetic material to ensue disease propagation. Small extracellular vesicles are produced via the endocytic pathways and released by nearly all cell types, including neurons. Due to their intrinsic interrelationship with endocytic processes and autophagy, there has been increased interest in studying the role of these neuronally-derived extracellular vesicles (NDEVs) in the propagation of AD. Pathologic cargo associated with AD have been found in a number of studies, and NDEVs have been shown to induce pathogenesis in vivo and in vitro. Exogenous NDEVs are also shown to reduce plaque burden in AD models. Thus, the NDEV has the potential to become a useful biomarker, a pathologic potentiator, and a therapeutic opportunity. While the field of NDEV research in AD is still in its infancy, we review the current literature supporting these three claims.
KW - Autophagy
KW - Beta-amyloid
KW - Cognitive impairment
KW - Dementia
KW - Exosome
KW - Mammalian target of rapamycin
KW - Neurodegeneration
KW - Tau
UR - http://www.scopus.com/inward/record.url?scp=85067170493&partnerID=8YFLogxK
U2 - 10.1186/s13024-019-0317-5
DO - 10.1186/s13024-019-0317-5
M3 - Review article
C2 - 31182115
AN - SCOPUS:85067170493
SN - 1750-1326
VL - 14
JO - Molecular Neurodegeneration
JF - Molecular Neurodegeneration
IS - 1
M1 - 22
ER -