Parkinson's Movement

cognitive dysfunctions, norepinephrine, atomoxetine, exercise

Dopamine is not the only significant neurotransmitter in PD.

The emerging

role of norepinephrine in cognitive dysfunctions of Parkinson's


Vazey EM, Aston-Jones G.


Behav Neurosci 2012 Jul 25;6:48.

Neuropathological studies demonstrate significant damage in brain

regions outside the nigral dopamine (DA) system, including early

degeneration of locus coeruleus norepinephrine (LC-NE) neurons, yet

discussion of PD and treatment focus has remained

dopaminergic-based. Motor symptoms benefit from DA replacement for

many years, but other symptoms including several cognitive deficits

continue unabated. Recent interest in non-DA substrates of PD

highlights early involvement of LC-NE neurons and provides evidence

for a prodromal phase, with cognitive disturbance, even in sporadic



disease as a system-level disorder.

NPJ Parkinsons

Dis 2016 Dec 1;2:16025.

Traditionally, the basal ganglia have been considered the main brain

region implicated in Parkinson's disease. This single area

perspective gives a restricted clinical picture and limits

therapeutic approaches because it ignores the influence of altered

interactions between the basal ganglia and other cerebral components

on Parkinsonian symptoms.


restores the response inhibition network in Parkinson's disease.


2016 Aug;139(Pt 8):2235-48.

These results suggest that (i) atomoxetine increases sensitivity of

the inferior frontal gyrus to afferent inputs from the

pre-supplementary motor cortex; (ii) atomoxetine can enhance

downstream modulation of frontal-subcortical connections for

response inhibition; and (iii) the behavioural consequences of

treatment are dependent on fronto-striatal structural connections.

The individual differences in behavioural responses to atomoxetine

highlight the need for patient stratification in future clinical

trials of noradrenergic therapies for Parkinson's disease.


Enhances Connectivity of Prefrontal Networks in Parkinson's



2016 Jul;41(8):2171-7.

Patients on placebo had reduced connectivity relative to controls

from right IFG to dorsal anterior cingulate cortex and to left IFG

and dorsolateral prefrontal cortex. Atomoxetine increased

connectivity from the right IFG to the dorsal anterior cingulate. In

addition, the atomoxetine-induced change in connectivity from right

IFG to dorsolateral prefrontal cortex was proportional to the change

in verbal fluency, a simple index of executive function.


benefits brain function: the monoamine connection.

Lin TW, Kuo YM.

Brain Sci 2013 Jan


The beneficial effects of exercise on brain function have been

demonstrated in animal models and in a growing number of clinical

studies on humans. There are multiple mechanisms that account for

the brain-enhancing effects of exercise, including

neuroinflammation, vascularization, antioxidation, energy

adaptation, and regulations on neurotrophic factors and

neurotransmitters. Dopamine (DA), noradrenaline (NE), and serotonin

(5-HT) are the three major monoamine neurotransmitters that are

known to be modulated by exercise. This review focuses on how these

three neurotransmitters contribute to exercise affecting brain

function and how it can work against neurological disorders.

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I was just reading today about Attention Deficit Hyperactivity Disorder (ADHD). It's interesting that it has been related to a deficiency in dopamine and norepinephrine.

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