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Motor symptoms of resting tremor, rigidity, bradykinesia, postural
instability and gait freezing are characteristic of Parkinson's disease (PD).
Non-motor symptoms are also
frequently present in PD, and are well
recognised as a major cause of disability.
They include fatigue, depression, sleep
disturbances, constipation and pain, with
dementia common in the later stages.
PD generally develops insidiously, and
is a neurodegenerative disorder due to
a deficiency in dopamine from selective
loss of dopaminergic neurons in the
substantia nigra, which also leads to
relative cholinergic excess in the brain.
An estimated 1% of people worldwide
(age adjusted) are living with PD. While
the mean age of onset for PD is 65 years
and prevalence is more common with
increasing age, younger people (<21 years
of age) have also been diagnosed with PD.
Pharmacological treatment of PD is
used to minimise symptoms, and is
reserved for when symptoms become
socially or physically disabling. Generally
speaking, these medications work to
increase dopamine or reduce cholinergic
excess. Levodopa, which is converted
into dopamine, is one of the first-line
treatment options. It is available
with either benserazide (Madopar),
or carbidopa (Sinemet), or carbidopa and
entacapone (Stalevo). Benserazide and
carbidopa reduce conversion of levodopa
in peripheral tissues, while entacapone,
which can be used as monotherapy,
inhibits an enzyme that degrades
dopamine. Dopamine agonists such as
pramipexole (Sifrol) and bromocriptine
(Kripton) can also be considered for
first-line therapy. Other medications
used include monoamine oxidase type B
inhibitors, which block one of the enzymes
involved in breaking down dopamine
(e.g. rasagiline, Azilect; selegiline, Selgene),
and anticholinergics (e.g. benzhexol,
Artane; benztropine, Benztrop).
Amantadine (Symmetrel), is also used
for PD, and increases dopamine release
while blocking cholinergic receptors.
Nutraceuticals (e.g. black tea, green tea,
caffeine) have also been identified from
large-scale epidemiological studies as
being 'possibly effective' for decreasing
the risk of PD, delaying the onset of PD,
or slowing the functional decline of PD.
Unfortunately, available treatment to date
is only for symptom management, and
no medication has been proven to slow
the progression of PD. However, recent
research in mouse models has suggested
that a humble spice commonly found in
the kitchen -- cinnamon -- may hold the
key to offering new hope for people living
Cinnamon is used as a spice and flavouring
agent in food and beverages. It has also
been suggested for use in a range of
ailments such as gastrointestinal upsets,
common cold, dysmenorrhea, bacterial
and helmintic infections, and stimulating
appetite, with varying levels of evidence
(or lack thereof ), to support its therapeutic
effectiveness in these conditions.
The active constituent of cinnamon is
thought to be its volatile oils. The volatile
oils are estimated to contain 60--80%
cinnamaldehyde, which reportedly have
a stimulant effect on the central nervous
system at low doses, and a sedative
effect at high doses. It is also touted to
have weak antipyretic, antibacterial,
antifungal, and hypothermic effects,
in addition to increasing peripheral blood
flow, reducing heart rate and blood
OLD DRUG NEW INDICATION
Dr Esther Lau is a Lecturer at the School of Clinical
Sciences, Queensland University of Technology.
Professor Lisa Nissen is Head of the School of Clinical
Sciences, Queensland University of Technology.
pressure, and having an effect on blood
sugar levels. Other constituents found in
cinnamon include tannins, thought to be
responsible for anti-diarrhoeal effects, and
methylhydroxychalcone polymer which
may improve insulin sensitivity.
Recent in vitro and in vivo animal studies
have suggested that cinnamon may show
potential for halting the progression of
PD. It is hypothesised that these effects
are through up-regulating and preventing
the loss of proteins such as Parkin and
DJ-1, which stimulate and support the
survival of remaining dopaminergic
neurons in the substantia nigra, as people
with PD have decreased levels of these
proteins. Solutions of dissolved cinnamon
(100 mg/kg body weight/day for seven
days), and its metabolite sodium benzoate
(50 mg/kg body weight/day for seven days)
were administered orally to mouse models
of PD, and showed promising results in
protecting and preventing the loss of Parkin
and DJ-1. The researchers hypothesised that
these effects were due to sodium benzoate,
a metabolite of cinnamon, which prevented
the loss of Parkin and DJ-1, protected
dopaminergic neurons, normalised striatal
neurotransmitter levels, and improved
motor functions. Using cinnamon to halt PD
is still in the early stages of testing in animal
models, and more research is required to
determine an appropriate oral dose for
human use. If future research can show that
these results can be translated to humans,
then cinnamon could pave the way as a safe
and cost-effective way to treat and halt the
progression of PD.
1. Khasnavis S, Pahan, K. Cinnamon treatment upregulates
neuroprotective proteins Parkin and DJ-1 and protects
dopaminergic neurons in a mouse model of Parkinson's
disease. J Neuroimmune Pharmacol. 2014;9(4):569--81.
2. Khasnavis S, Pahan, K. Sodium benzoate, a metabolite of
cinnamon and a food additive, upregulates neuroprotective
Parkinson disease protein DJ-1 in astrocytes and neurons. J
Neuroimmune Pharmacol. 2012;7(2):424--35.
3. Paterna JC, Leng A, Weber E, Feldon J, Bueler H. DJ-1 and
Parkin modulate dopamine-dependent behaviour and
inhibit MPTP-induced nigral dopamine neuron loss in mice.
Mol Ther. 2007;15(4):698--704.
4. Jana A, Modi KK, Roy A, Anderson JA, van Breemen RB, Pahan
K. Up-regulation of neurotrophic factors by cinnamon and
its metabolite sodium benzoate: therapeutic implications for
neurodegenerative disorders. J Neuroimmune Pharmacol.
A bit of spice for Parkinson's
BY PROFESSOR LISA NISSEN & DR ESTHER LAU
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