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Vesicular Acetylcholine Transporter (VAChT) &
Vesicular Monoamine Transporter (VMAT 2)
Recent studies support that Alzheimer's disease has an age-related interplay between Aβ accumulation, cholinergic dysfunction, and vascular impairments.
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Regulation of cholinergic activity by the vesicular acetylcholine transporter.

Acetylcholine, the first chemical to be identified as a neurotransmitter, is packed in synaptic vesicles by the activity of VAChT (vesicular acetylcholine transporter). A decrease in VAChT expression has been reported in a number of diseases, and this has consequences for the amount of acetylcholine loaded in synaptic vesicles as well as for neurotransmitter release. Several genetically modified mice targeting the VAChT gene have been generated, providing novel models to understand how changes in VAChT affect transmitter release. A surprising finding is that most cholinergic neurons in the brain also can express a second type of vesicular neurotransmitter transporter that allows these neurons to secrete two distinct neurotransmitters. Thus a given neuron can use two neurotransmitters to regulate different physiological functions. In addition, recent data indicate that non-neuronal cells can also express the machinery used to synthesize and release acetylcholine. Some of these cells rely on VAChT to secrete acetylcholine with potential physiological consequences in the periphery. Hence novel functions for the oldest neurotransmitter known are emerging with the potential to provide new targets for the treatment of several pathological conditions.

Prado VF et al, Biochem J. 2013 Mar 1;450(2):265-74. doi: 10.1042/BJ20121662.

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β-Amyloid, Cholinergic Transmission, And Cerebrovascular System - A Developmental Study In A Mouse Model Of Alzheimer's Disease.

Kuznetsova E, Schliebs R, Curr Pharm Des. 2013 Mar 19. [Epub ahead of print]

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Mice with selective elimination of striatal acetylcholine release are lean, show altered energy homeostasis and changed sleep/wake cycle.

Guzman MS et al, J Neurochem. 2013 Mar;124(5):658-69. doi: 10.1111/jnc.12128. Epub 2013 Jan 15.

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Overexpression of the vesicular acetylcholine transporter increased acetylcholine release in the hippocampus.

Nagy PM, Aubert I et al, Neuroscience. 2012 Aug 30;218:1-11. doi: 10.1016/j.neuroscience.2012.05.047.

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A panel of cerebrospinal fluid potential biomarkers for the diagnosis of Alzheimer's disease

Carrette O at el. Proteomics. 2003 Aug;3(8):1486-94.

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Synaptic proteins in Alzheimer's disease

Marksteiner J at el. J Mol Neurosci. 2002 Feb-Apr;18(1-2):53-63.

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Chemical neuroanatomy of the vesicular amine transporters

Eberhard Weihe and Lee E. Eiden. FASEB J. 14, 2435-2449 (2000)

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Synaptic loss reflected by secretoneurin-like immunoreactivity in the human hippocampus in Alzheimer's disease 

Kaufmann WA at el. Eur J Neurosci. 1998 Mar;10(3):1084-94.

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Levels and proteolytic processing of chromogranin A and B and secretogranin II in cerebrospinal fluid in neurological diseases

Eder U at el. J Neural Transm. 1998;105(1):39-51.

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Synaptic pathology in Alzheimer's disease: immunological data for markers of synaptic and large dense-core vesicles

Lassmann H at el. Neuroscience. 1992;46(1):1-8.

 

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