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2014 ; 14
(10
): 1115-7
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VMAT2 and Parkinson s disease: harnessing the dopamine vesicle
#MMPMID25220836
Lohr KM
; Miller GW
Expert Rev Neurother
2014[Oct]; 14
(10
): 1115-7
PMID25220836
show ga
Despite a movement away from dopamine-focused Parkinson's disease (PD) research,
a recent surge of evidence now suggests that altered vesicular storage of
dopamine may contribute to the demise of the nigral neurons in this disease.
Human studies demonstrate that the vesicular monoamine transporter 2 (VMAT2;
SLC18A2) is dysfunctional in PD brain. Moreover, studies with transgenic mice
suggest that there is an untapped reserve capacity of the dopamine vesicle that
could be unbridled by increasing VMAT2 function. Therapeutic manipulation of
VMAT2 level or function has the potential to improve efficacy of dopamine derived
from administered levodopa, increase dopamine neurotransmission from remaining
midbrain dopamine neurons and protect against neurotoxic insults. Thus, the
development of drugs to enhance the storage of release of dopamine may be a
fruitful avenue of research for PD.
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