Effects of long-term administration of a cocoa polyphenolic extract
(Acticoa powder) on cognitive performances in aged rats
Jean-Franc ¸ois Bisson1, Amine Nejdi1, Pascale Rozan1, Sophie Hidalgo1, Robert Lalonde2
and Michae ¨l Messaoudi1*
1ETAP-Applied Ethology, 13 rue du Bois de la Champelle, Vandoeuvre-le `s-Nancy 54500, France
2CHUM/St-Luc, Neuroscience Research Center, 1058 St-Denis Street, Montre ´al H2X 3J4, PQ, Canada
(Received 29 May 2007 – Revised 13 September 2007 – Accepted 2 November 2007 – First published online 8 January 2008)
Numerous studies have indicated that increased vulnerability to oxidative stress may be the main factor involved in functional declines during
normal and pathological ageing, and that antioxidant agents, such as polyphenols, may improve or prevent these deficits. We examined whether
1-year administration of a cocoa polyphenolic extract (Acticoa powder), orally delivered at the dose of 24mg/kg per d between 15 and 27 months
of age, affects the onset of age-related cognitive deficits, urinary free dopamine levels and lifespan in old Wistar-Unilever rats. Acticoa powder
improved cognitive performances in light extinction and water maze paradigms, increased lifespan and preserved high urinary free dopamine
levels. These results suggest that Acticoa powder may be beneficial in retarding age-related brain impairments, including cognitive deficits in
normal ageing and perhaps neurodegenerative diseases. Further studies are required to elucidate the mechanisms of cocoa polyphenols in neuro-
protection and to explore their effects in man.
Cocoa polyphenols: Cognitive performances: Ageing: Lifespan: Rats
Because of their post-mitotic nature, neurons contend with cel-
lular damage accumulated over many decades. The brain is
more vulnerable to oxidative stress than other organs due to
its low antioxidant protection system and increased exposure
of target molecules to reactive oxygen species, one of the
major damaging agents involved in age-associated decline(1).
Increased reactive oxygen species levels produced by mito-
chondrial activity, inflammatory processes and excessive glu-
parameters related to neurotransmission also decline during
Numerous epidemiological studies indicate that dietary
flavonoids derived from fruits, vegetables, red wine and
green tea decrease the risk of death from CHD(6,7), cancer(8)
and stroke(9), and may prevent neurodegenerative diseases
and diabetes mellitus(10). Only recently have the beneficial
effects of dietary polyphenols come to the attention of nutri-
tionists(11). Polyphenols are present in plants in the form of
non-conjugated molecules, including (2)-epicatechin and
(þ)-catechin, as well as their oligomers, also named procyani-
dins(12–14). Cocoa-derived products contain high levels of
flavonoids(12,15,16)and show potent antioxidant effects(17).
Biomarkers associated with CVD, such as oxidant defence
molecules, LDL oxidation state and platelet function, have
been assessed after acute consumption of chocolate and
cocoa(18–20). The increase in blood epicatechin after acute pro-
cyanidin-rich chocolate consumption was associated with
increased plasma antioxidant capacity and decreased plasma
2-thiobarbituric acid reactive substances(20). In addition, (þ)-
catechin and (2)-epicatechin delayed lipid oxidation as well
as depleted a-tocopherol and b-carotene levels induced by a
free radical generator in human oxidized plasma(21). It was
shown that consumption of green tea prevented LDL oxidation
in man(22)and that tea catechins attenuated the development of
atherosclerosis in apoE-deficient mice(23). The antioxidant
properties of polyphenols and their beneficial effects on cogni-
tion have been demonstrated in animal studies(24). There is a
possible role for (2)-epicatechin in reducing neurodegene-
diseases(25,26). Polyphenols may also possess other types of
The main purpose of the present study was to investigate
the effects of Acticoa powder, a cocoa polyphenolic extract,
on cognitive function and lifespan in aged Wistar-Unilever
rats, assessed with light extinction(29–31)and water maze
tests, the latter adapted from Morris(32)in which rats were
let go from the same starting position. The rats were also eval-
uated for urinary free dopamine levels, susceptible to age-
related decreases in Wistar rats(33).
Materials and methods
Eighteen male Wistar-Unilever rats (Harlan, The Nether-
lands), weighing 250–275g at reception, were housed three
*Corresponding author: Dr Michae ¨l Messaoudi, fax þ33 383 446 441, email firstname.lastname@example.org
Abbreviation: AP24, Acticoa powder (24mg/kg per d).
British Journal of Nutrition (2008), 100, 94–101
q The Authors 2007
British Journal of Nutrition
per cage in 48 £ 27 £ 20cm polycarbonate cages (U.A.R.,
Epinay-Sur-Orge, France) in a regulated environment (tem-
perature 22 ^ 28C; humidity 50 ^ 10%), provided standard
food (food pellets M20; Dietex, Saint Gratien, France) and
tap water ad libitum, and maintained on a 12h light/dark
cycle (lights on 20.00–08.00 hours).
After an 8-month acclimatization period in our facility, the
rats were matched according to weight and randomly assigned
to one of two groups (n 9): control-vehicle or Acticoa powder
(cocoa polyphenolic extract) at the dose of 24mg/kg per d
(AP24), given by oral gavage. The rats were tested for cogni-
tive functions at 9, 13 and 15 months, received AP24 or its
vehicle (spring water), and were then retested at 17, 21 and
25 months for light extinction and water maze tests.
The rats used in the present study were treated according to
rules provided by the ASAB Ethical Committee (1993) and
the Canadian Council on Animal Care (1993). All standard
operating procedures were in compliance with the European
Communities Council Directive 86/609/EEC of 24 November
1986 on the approximation of laws, regulations and adminis-
trative provisions of the Member States regarding the protec-
tion of animals used for scientific purposes (Official Journal L
358, 18 December 1986, pp. 0001–0028).
The solvent-free Acticoa powder was provided by Barry Call-
ebaut France (Louviers, France). It was isolated from non-
roasted beans using the patented Acticoa process recently
developed by Barry Callebaut France. The general compo-
sition of AP24 was as follows (g/100g): 3·5g moisture,
29·4g proteins, 13·2g fat, 12·8g carbohydrates, 3·8g fibres,
2·4g minerals and 34·9g total polyphenols. The percentages
related to the polyphenols in AP24 determined by HPLC
were 88·5% procyanidins including 0·21% anthocyanins,
10% epicatechin, 1% epicatechin gallate and 0·5% catechin.
The product was freshly prepared every day; it was dissolved
in spring water and administered at a dose of 24mg/5ml per
kg body weight. AP24 and vehicle were orally administered
for 12 months from the age of 15–27 months. After daily
administration, the rats were allowed free access to standard
food pellets and were weighed three times per week.
Only a single dosage of AP24 was investigated on the basis
of results from a chronic experiment which showed its ben-
eficial effects on prostate cancer prevention in rats(34).
Weight change and food and water consumption.
weight of each rat was recorded three times per week during
the whole experimental period. Food and water consumption
were recorded every week from Monday to Friday, for each
cage, in order to estimate the quantity of food and water
ingested by rats. Then the mean quantities of food and water
were calculated in g/100g body weight for rats of each cage
in the two groups.
Cognitive testing. All cognitive tests were recorded by
experimenters unaware of administered treatments.
Light extinction: light extinction was tested before treat-
ment at 9, 13 and 15 months of age and after treatment at
17, 21 and 25 months of age. Learning performance was
assessed by means of an operant conditioning test based on
the natural aversion of rats to bright light(29–31). The rat
was placed in a strongly illuminated (1200 lux) cage
(50 £ 40 £ 37cm) equipped with two levers. By pressing the
active lever the rat switched off the light allowing access to
a 30s period of darkness, whereas the inactive lever had no
effect on the environment. The test lasted 20min and the
number of active and inactive lever presses were recorded.
Water maze: at 8, 12 and 15 months of age, the rats were
trained to find a hidden platform (1cm beneath water surface
at 238C) in a tank (150cm diameter) filled with water from the
same starting position for five trials per test session with a
maximal duration of 180s for each trial. The platform was
placed away from the wall in a constant quadrant position
during the trials. On each trial, the rats were allowed to stay
on the platform for 30s and then were immediately placed
back in the water for the next trial. When unable to find the
platform, the rats were placed on it for the same amount of
time. At 17, 21 and 25 months of age, the rats were retested
under treatment or placebo with the same procedure. In our
simplified procedure, the rat is proficient in learning to
locate more quickly the hidden platform by memorizing its
position during a single five-trial session.
Urinary dopamine levels.Rats were individually placed in
metabolic cages for 7h from 09.00 to 16.00 hours for the
collection of urine samples. Urinary dopamine levels were
assayed at 12, 15, 18, 21, 24 and 27 months of age by
HPLC with electrochemical detection. Aliquots of 1·0ml acid-
ified urine were placed in 5ml conical-base glass vials with
50mg alumina, and the samples were adjusted to pH 8·6 by
adding Tris buffer. The adsorbed dopamine was then eluted
from the alumina with 200ml of 0·2mol/l HClO4on Costar
Spin-X microfilters. In the final phase, 50ml of the eluate
were injected into an HPLC apparatus (Gilson Medical Elec-
tronics, Villiers-le-Bel, France) with a minimal limit of detec-
tion of 4mg/l.
Throughout the experiment, the date of death of each rat was
noted in order to determine the mean lifespan in each group.
Due to the relatively small number of rats per group, which
decreased during the course of the study, and due to unequal
variances, non-parametric tests(35)were used. The Mann–
Whitney Utest was used to compare cognitive performances
of the two groups. For each group, the Friedman test was
employed to compare the repeated cognitive performances
throughout the test sessions; whenever significant, the Wil-
coxon test was used to compare the performances of two con-
secutive water maze tests and to evaluate lever discrimination
in the light extinction test by comparing the numbers of active
and inactive lever presses. Survival data were analysed using
the Kaplan–Meier method(36). The difference between survi-
val in the two groups was tested using the log rank test. All
statistical analyses were carried out with StatVieww5 soft-
ware (SAS Inc., Cary, NC, USA). The results are expressed
as means and their standard errors. Differences were con-
sidered to be significant at P,0·05.
Cocoa polyphenolic extract and ageing95
British Journal of Nutrition
Weight change and food and water consumption
No significant differences were observed between the body
weight and food and water consumption of the two groups
recorded throughout the study period (data not shown).
significant group differences were apparent for total number of
lever presses prior to Acticoa powder or vehicle adminis-
tration at 9, 13 and 15 months of age (Mann–Whitney
Utest: U 29·50, NS; U 24·00, NS; U 31·50, NS, respectively).
But at 17, 21 and 25 months of age, total lever pressing
activity was significantly more elevated in AP24-treated rats
(Mann–Whitney Utest: U 13·0, P,0·03; U 4·50, P,0·004;
U 5·00, P,0·04, respectively).
Lever discrimination: as shown in Fig. 2, control rats (treated
with the vehicle) failed to show a significant discrimination
between the two levers during baseline at 9, 13 and 15
months (Wilcoxon test: z 0·95, NS; z 1·27, NS; z 0·68, NS,
respectively) and during the treatment period at 17, 21 and 25
months (Wilcoxon test: z 0·43, NS; z 0·65, NS; z 0·38, NS,
respectively). Although AP24-treated rats did not discriminate
between the two levers at baseline (Wilcoxon test: z 0·34, NS;
z 0·57, NS; z 1·02, NS, respectively), lever discrimination was
observed at 17 and 21 months (Wilcoxon test: z 2·32, P,0·02;
z 2·68, P,0·008, respectively). But at 25 months, presses on
the active lever only tended to be higher than those on the inac-
tive one (Wilcoxon test: z 1·70, P,0·09).
Water maze.Global performances: during baseline at 8,
12 and 15, and during treatment at 17 months of age, no inter-
group differences were found for escape latencies (Mann–
Whitney Utest: U 34·50, NS; U 32·50, NS; U 35, NS;
U 20·5, NS, respectively; Fig. 3). But at 21 and 25 months,
escape latencies of AP24-treated rats were significantly
Total lever presses: as shown in Fig. 1, no
lower than those of control rats (Mann–Whitney Utest:
U 6·00, P¼0·007; U 0·00, P¼0·006, respectively).
Long-term memory: long-term memory was evaluated by
comparing group performances over months using the Wil-
coxon test (Fig. 3). Both groups improved their performances
from month 8 to 12 (z 2·67, P,0·008 for AP24-treated rats;
z 2·52, P,0·02 for controls) and from month 8 to 15 (z 2·67,
P,0·008 for AP24-treated rats; z 2·52, P,0·02 for controls).
The performance of control rats was still stable from month 15
to 17 (z 0·154, NS), but significantly deteriorated at 21 and 25
months (z 2·37, P¼0·018; z 2·02, P¼0·043, respectively). In
contrast, the performance of AP24-treated rats was stable
from 15 to 17 (z 0·48, NS), from 15 to 21 (z 0·42, NS) and
from 15 to 25 (z 0·31, NS) months.
Short-term memory: short-term memory was assessed by
comparing group performances over daily trials (Fig. 4).
During the first water maze test at baseline, both groups
improved their escape latencies from trial 1 to trial 5 (Friedman
test: x2(4 df) 20·56, P¼0·0004 for AP24-treated rats; x2(4 df)
10·58, P¼0·03 for controls). During 12- and 15-month test ses-
sions (baseline), escape latencies of both groups remained low
throughout every trial to the extent that short-term memory
assessment became meaningless (month 12: x2(4 df) 7·17, NS
for AP24-treated rats; x2(4 df) 10·80, P¼0·03 for controls;
month 15: x2(4 df) 14·92, P¼0·005 for AP24-treated rats;
x2(4 df) 7·52, NS for controls) (Figs. 4 (A), (B) and (C)).
15 1721 25
Number of lever presses
(9)(9)(9)(9)(9)(9)(9)(8)(6) (7) (9)(9)
Fig. 1. Total number of lever presses (active þ inactive lever presses) in the
light extinction test before (9, 13 and 15 months) and after the start of treat-
ments (17, 21 and 25 months) in control rats (A) and in rats fed Acticoa pow-
der (24mg/kg per d; AP24;
). The numbers in parentheses are the number
of rats remaining in each group. Values are means with their standard errors
depicted by vertical bars. Mean values were significantly different from those
of the control group (Mann–Whitney U test): *P,0·05, **P,0·01.
Number of lever presses
Number of lever presses
Fig. 2. Discrimination between active ( ) and inactive (A) levers in the light
extinction test before (9, 13 and 15 months) and after the start of treatments
(17, 21 and 25 months) in control rats (A) and in rats fed Acticoa powder
(24mg/kg per d; AP24; B). Values are means with their standard errors
depicted by vertical bars. Mean values were significantly different from those
of the inactive levers (Wilcoxon test):TP,0·10, *P,0·05, **P,0·01.
J.-F. Bisson et al.96
British Journal of Nutrition
At the 17-month test session, AP24-treated and control rats
improved their latency to find the platform from trial 1 to trial
2 (z 2·67, P¼0·008; z 2·37, P¼0·018, respectively). Between
trial 2 and trial 5, latencies remained low and stable in the two
groups (Friedman test: x2(3 df) 2·87, NS; x2(3 df) 0·79, NS,
respectively). However, the performance of AP24-treated rats
was better than that of controls for trials 2, 3 and 4 (Fig. 4
(D)). At the 21- and 25-month test sessions, AP24-treated rats
improved their latencies on the first two trials (Wilcoxon test:
z 2·08, P¼0·04; z 2·07, P¼0·03, respectively) and between
trial2and trial5,their latenciesremainedlowandstable(Fried-
man test: x2(3 df) 4·01, NS; x2(3 df) 2·50, NS, respectively). In
contrast, latencies of control rats showed no improvement
between trial 1 and trial 5 (Friedman test: x2(4 df) 2·84, NS;
sions, the performance of AP24-treated rats was significantly
better than that of control rats (Figs. 4 (E) and (F)).
Urinary free dopamine
As seen in Fig. 5, urinary free dopamine concentrations
remained stable in the two groups from 12 to 15 months of
Fig. 3. Water maze performances before (8, 12 and 15 months) and after the
start of treatments (17, 21 and 25 months) in control rats (A) and in rats fed
Acticoa powder (24mg/kg per d; AP24;
latencies over five trials before finding the hidden platform in each test ses-
sion. Values are means with their standard errors depicted by vertical bars.
Mean values were significantly different from those of the AP24-treated rats
(Mann–Whitney U test): **P,0·01.
). Results are given as mean
T1 T2T3T4T5 T1T2T3T4T5
Fig. 4. Water maze performances at 8 (A), 12 (B), 15 months (C) (before treatment), and 17 (D), 21 (E) and 25 (F) (period of treatment) months of age in control
rats (W) and in rats fed Acticoa powder (24mg/kg per d; AP24; X). Results are given as mean latencies from the five trials of the test session (T1–T5). Mean
values were significantly different from those of the AP24-treated rats (Mann–Whitney U test):TP,0·10, *P,0·05, **P,0·01.
Cocoa polyphenolic extract and ageing97
British Journal of Nutrition
age and no group difference was discerned (Mann–Whitney
Utest: U 10, NS; U 6, NS, respectively). Urinary free dopa-
mine concentrations of AP24-treated rats were significantly
lower than those of control rats at 18 months of age (U 2,
P,0·02), but significantly higher at 24 and 27 months of
age (Mann–Whitney Utest: U 0, P,0·002; U 0, P,0·008,
in AP24-treated rats from 18 to 27 months (Friedman test:
x2(3 df) 0·80, NS), values of control rats tended to decline
(Friedman test: x2(3 df) 7·46, P,0·06).
The log-rank statistical test showed a significant increase of
survival times in the AP24-treated group in comparison to con-
trol rats (x2(1 df) 5·169, P¼0·025), corresponding to a longer
lifespan of about 11% over the 27-month period (Fig. 6).
The main purpose of the present work was to determine
whether a daily dose of Acticoa powder ingested by aged
rats over a 12-month period retards the onset of age-related
cognitive deficits. In the light extinction test, AP24-treated
rats had more total lever pressing activity than control rats.
Moreover, unlike placebo-treated controls, AP24-treated rats
exhibited significant discrimination between active and inac-
tive levers at 17 and 21 months of age. The reason why control
rats failed to discriminate is uncertain. We previously
observed significant lever discrimination in 3-month-old
male Wistar rats(29–31). We suspect that age level is critical
and it should be interesting to evaluate younger Wistar-Unile-
ver rats in the same paradigm. It remains to be determined
whether the elevated lever activity of AP24-treated rats is gen-
eralizable to exploratory activity in the open-field and hole-
board, susceptible to decline as a result of advanced ageing
in rats and mice(37). It also remains to be determined why
the AP24 group discriminates. One possiblity is faciliation
of cognitive processes. A second possibility is that light is
more aversive to them. There is a need to assess the effects
of this substance on photophobia and other anxiety tests.
While water maze performance declined in control rats at
21 and 25 months of age, it remained stable in AP24-treated
rats. At 21 and 25 months, but not at 17 months, escape
latencies of AP24-treated rats were lower than those of control
rats. Both long- and short-term memory processes were
improved by the cocoa polyphenolic extract, as evaluated by
month-to-month or trial-to-trial performances. The present
results demonstrate beneficial effects of Acticoa powder on
Many studies indicate that age-associated neurobehavioural
deficits are attenuated by dietary supplementation with potent
antioxidant activity, such as Ginkgo biloba flavonoids, includ-
ing memory(38), attention(39)and calcium-induced increases in
oxidative metabolism(40). It may be possible to reduce the
deleterious effects of Alzheimer’s disease with such sup-
plements(41)or at least delay the physiological impairment
associated with normal ageing(42). In particular, Moriguchi
et al.(43)reported that a garlic extract prevented brain atrophy,
as well as learning and memory impairments in the senescence
The present results are in accordance with those of Joseph
et al.(24)concerning the beneficial action of dietary sup-
plementation with spinach, strawberry and blueberry extracts
high in flavonoid levels as well as antioxidant activity(45)on
neuronal and cognitive functions in aged rats. Moreover,
age-related declines in spatial memory tasks and hippocampal
plasticity parameters were improved by antioxidant-rich
diets containing blueberries(46,47). Likewise, tea polyphenols
immediately after ischaemia improved memory impairment
and reduced hippocampal damage in mice(48)and in ger-
bils(49). In the mouse hippocampal model system for oxidative
stress, many flavonoids protected HT-22 cells from glutamate-
induced toxicity as well as other oxidative insults(50).
Urinary free dopamine
Dopamine is an essential neurotransmitter enabling smooth,
controlled movements as well as efficient memory, attention
121518 2124 27
Fig. 5. Urinary free dopamine concentrations before (12 and 15 months) and
after the start of treatments (18, 21, 24 and 27 months) in control rats (A)
and in rats fed Acticoa powder (24mg/kg per d; AP24;
parentheses are the number of rats remaining in each group. Values are
means with their standard errors depicted by vertical bars. Mean values were
significantly different from those of the control group (Mann–Whitney U test):
). The numbers in
Survival rate (%)
Fig. 6. Survival rates of control rats ( ) and rats fed Acticoa powder
(24mg/kg per d; AP24; X). Survival times of rats were analysed using the
Kaplan–Meier method and the log-rank test.
J.-F. Bisson et al.98
British Journal of Nutrition
and problem-solving function. Three months after the start of
the treatment period, urinary free dopamine levels were para-
doxically much higher in control than AP24-treated rats. At 21
months of age (6 months of treatment), no significant differ-
ence was observed between the dopamine levels of the two
groups. At 24 and 27 months of age, urinary dopamine con-
centration declined in control rats, but remained relatively
high and stable in AP24-treated rats. On the basis of the pre-
sent results, the variability of urinary dopamine is probably
not due to the salt content in the extract. Urinary dopamine
levels exhibited by control rats are concordant with the age-
related decrease found in Wistar rats(33). Some studies directly
associate the level of free dopamine in urine with the severity
of the Parkinsonian syndrome(51,52). Hoehnetal.(52)concluded
that, although many peripheral sources contribute to urinary
free dopamine, asmall decrease in thelevel may actually reflect
the severity of the disturbance of central dopamine metabolism
and the known deficiency of dopamine in the neurons of the
Parkinsonian brain. Green tea polyphenols inhibited the
uptake of [3H]dopamine and 1-methyl-4-phenylpyridinium by
dopamine transporters and partially protected embryonic rat
mesencephalic dopaminergic neurons from 1-methyl-4-phenyl-
pyridinium-induced injury(53). Similarly, potent neuroprotec-
tive properties of green tea polyphenols were demonstrated
with respect to striatal dopamine depletion and substantia
nigra dopaminergic neuronal loss caused by 1-methyl-
oxygen species are involved in the decline of functions associ-
ated with ageing(1)and flavonoid administration attenuated
apoptotic injury of mesencephalic dopamine neurons caused
by oxidative stress(55). Joseph et al.(24)examined the brain tis-
sues of blueberry-supplemented rats and found that dopamine
levels were significantly higher than those of control rats.
Despite distinct chemical structures, cocoa antioxidant
effects are similar to those of tea or blueberry, providing
antioxidant defences against reactive oxygen species(12,56).
Cocoa polyphenol extracts may therefore protect vulnerable
structures such as the nigro-striatal system against dopamine
The lifespan of AP24-treated rats was prolonged relative to
placebo by approximately 11% over the 27-month test
period. The mechanisms underlying prolongation of the life-
span of the Acticoa powder remain to be fully established. It
was demonstrated that cocoa powder enhances the level of
antioxidative activity in rat plasma(62,63)and among human
subjects, a flavonoid-rich chocolate increased plasma antioxi-
dant capacity and reduced the amounts of plasma 2-thiobarbi-
turic acid-reactive substances(64). Lee et al.(65)showed that
cocoa powder and cocoa extracts exhibit greater antioxidant
capacity than many other flavanol-rich foods and food
extracts, such as green and black tea, and red wine.
However, the beneficial effects of the cocoa extract are
attributable not only to antioxidant properties of its polyphenol
constituents (procyanidins and methylxanthines), but also
via inhibition of nitric oxide-stimulated protein kinase C
activity, since flavanols improved nitric oxide-dependent
vasodilatation even in the presence of pre-existing endothelial
dysfunction(66,67). Cocoa polyphenols may improve vasodilata-
tion, dependent on epicatechin(68). The cocoa polyphenolic
improved endothelium-dependent relaxation(71), modulation of
cytokines and eicosanoids involved in the inflammatory
response(72–74), and inhibition of platelet activation(20,75,76).
Since AP24 administration did not show any influence on
weight and on food and water consumption of treated rats
throughout the experimental period, the benefits observed
with the AP24 cocoa extract are not due to dietary restriction.
The present results suggest that Acticoa powder may be ben-
eficial in retarding age-related brain impairments, including
cognitive deficits in normal ageing and perhaps neurodegen-
erative diseases. On the basis of the present results, it is of
interest to carry out further in-depth preclinical and clinical
studies on the neurobehavioural actions of Acticoa powder
in order to determine whether age-related dysfunctions may
be prevented and to elucidate the mechanisms of cocoa poly-
phenols in neuroprotection.
We are grateful to the Barry Callebaut Group (France) for sup-
plying Acticoa powder samples. J.-F. B., M. M. and S. H.
were responsible for performing the study. M. M., A. N. and
P. R. were responsible for data management and statistical
expertise. J.-F. B., M. M., A. N. and P. R. were also respon-
sible for data interpretation and manuscript writing. R. L. con-
tributed to data interpretation and manuscript writing. There
were no conflicts of interest.
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