Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 70, Issue -, Pages 21-35Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2018.03.020
Keywords
Dopamine transporter; Parkinson's Disease; Macrophages; Dopamine; Peripheral immunity
Categories
Funding
- NIDA NIH HHS [R01 DA039005, R01 DA026947, R21 DA043895] Funding Source: Medline
- NIMH NIH HHS [T32 MH079785] Funding Source: Medline
- NINDS NIH HHS [T32 NS082168, R01 NS071122] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS071122, T32NS082168] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA026947, R21DA043895] Funding Source: NIH RePORTER
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The second-most common neurodegenerative disease, Parkinson's Disease (PD) has three hallmarks: dysfunctional dopamine transmission due, at least in part, to dopamine neuron degeneration; intracellular inclusions of alpha-synuclein aggregates; and neuroinflammation. The origin and interplay of these features remains a puzzle, as does the underlying mechanism of PD pathogenesis and progression. When viewed in the context of neuroimmunology, dopamine also plays a role in regulating peripheral immune cells. Intriguingly, plasma dopamine levels are altered in PD, suggesting collateral dysregulation of peripheral dopamine transmission. The dopamine transporter (DAT), the main regulator of dopaminergic tone in the CNS, is known to exist in lymphocytes and monocytesimacrophages, but little is known about peripheral DAT biology or how DAT regulates the dopaminergic tone, much less how peripheral DAT alters immune function. Our review is guided by the hypothesis that dysfunctional peripheral dopamine signaling might be linked to the dysfunctional immune responses in PD and thereby suggests a potential bidirectional communication between central and peripheral dopamine systems. This review seeks to foster new perspectives concerning PD pathogenesis and progression. (C) 2018 Elsevier Inc. All rights reserved.
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