Dopamine is not the only significant neurotransmitter in PD.
The emerging
role of norepinephrine in cognitive dysfunctions of Parkinson's
disease.
Vazey EM, Aston-Jones G.
Front
Behav Neurosci 2012 Jul 25;6:48.
ncbi.nlm.nih.gov/pmc/articl...
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
PD.
Parkinson's
disease as a system-level disorder.
NPJ Parkinsons
Dis 2016 Dec 1;2:16025.
ncbi.nlm.nih.gov/pmc/articl...
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.
Atomoxetine
restores the response inhibition network in Parkinson's disease.
Brain
2016 Aug;139(Pt 8):2235-48.
ncbi.nlm.nih.gov/pubmed/273...
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.
Atomoxetine
Enhances Connectivity of Prefrontal Networks in Parkinson's
Disease.
Neuropsychopharmacology
2016 Jul;41(8):2171-7.
ncbi.nlm.nih.gov/pmc/articl...
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.
Exercise
benefits brain function: the monoamine connection.
Lin TW, Kuo YM.
Brain Sci 2013 Jan
11;3(1):39-53.
ncbi.nlm.nih.gov/pmc/articl...
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.