Abstract
This
paper discusses the effects of curcumin on patients with Alzheimer's
disease (AD). Curcumin (Turmeric), an ancient Indian herb used in curry
powder, has been extensively studied in modern medicine and Indian
systems of medicine for the treatment of various medical conditions,
including cystic fibrosis, haemorrhoids, gastric ulcer, colon cancer,
breast cancer, atherosclerosis, liver diseases and arthritis. It has
been used in various types of treatments for dementia and traumatic
brain injury. Curcumin also has a potential role in the prevention and
treatment of AD. Curcumin as an antioxidant, anti-inflammatory and
lipophilic action improves the cognitive functions in patients with AD. A
growing body of evidence indicates that oxidative stress, free
radicals, beta amyloid, cerebral deregulation caused by bio-metal
toxicity and abnormal inflammatory reactions contribute to the key event
in Alzheimer's disease pathology. Due to various effects of curcumin,
such as decreased Beta-amyloid plaques, delayed degradation of neurons,
metal-chelation, anti-inflammatory, antioxidant and decreased microglia
formation, the overall memory in patients with AD has improved. This
paper reviews the various mechanisms of actions of curcumin in AD and
pathology.
Keywords: Alternative approach to Alzheimer's, beta amyloid plaques, curcumin, curcumin and dementia, epidemiology, turmeric
Introduction
Alzheimer's disease
Alzheimer's
disease (AD) is a progressive neurodegenerative disease. It is
characterized by progressive cognitive deterioration together with
declining activities of daily living and behavioral changes. It is the
most common type of pre-senile and senile dementia. According to the
World Health Organization (WHO), 5% of men and 6% of woman of above the
age of 60 years are affected with Alzheimer's type dementia worldwide.[
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In India, the total prevalence of dementia per 1000 people is 33.6%, of
which AD constitutes approximately 54% and vascular dementia
constitutes approximately 39%. AD affects approximately 4.5 million
people in the United States or approximately 10% of the population over
the age of 65, and this number is projected to reach four times by 2050.
The frequency increases to 50% by the age of 80 years. Every year more
than $100 billion is spent for health care in the U.S. to treat AD in
primary care settings alone.Neuropathology of AD:
The
neuropathological process consists of neuronal loss and atrophy,
principally in the temporoparietal and frontal cortex, with an
inflammatory response to the deposition of amyloid plaques and an
abnormal cluster of protein fragments and tangled bundles of fibres
(neurofibillary tangles). Neurotic plaques are relatively insoluble
dense cores of 5-10 nm thick amyloid fibrils with a pallor staining
“halo” surrounded by dystrophic neuritis, reactive astrocytes and
activated microglia. There is an increased presence of
monocytes/macrophages in the cerebral vessel wall and reactive or
activated microglial cells in the adjacent parenchyma.[
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Destroy user interface control3] The main protein component of amyloid in AD is the 39-42 amino acid (beta) amyloid peptide (A-beta) [Figure 1].
Neuritic plaques are one of the characteristic structural abnormalities found in the brains of Alzheimer patients
Curcumin
Curcumin (Curcuma longa - Haldi) is the source of the spice Turmeric [Figure 2]
and is used in curries and other spicy dishes from India, Asia and the
Middle East. Similar to many other herbal remedies, people first used
curcumin as a food and later discovered that it also had impressive
medicinal qualities. It has been used extensively in Ayurveda (Indian
system of Medicine) for centuries as a pain relieving, anti-inflammatory
agent to relieve pain and inflammation in the skin and muscles. It has
also proven to have anti-cancer properties.[
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Curcumin holds a high place in Ayurvedic medicine as a “cleanser of the
body,” and today, science is finding a growing list of diseased
conditions that can be healed by the active ingredients of turmeric.[
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(2a) Turmeric, (2b) Turmeric plant, (2c) Keto and enol form of curcumin
The Plant
Botanical
name: Curcuma longa; Family: Zingiberaceae, the ginger family. Turmeric
is a sterile plant and does not produce any seeds [Figure 2].
The plant grows up to 3-5 ft tall and has dull yellow flowers. The
underground rhizomes or roots of the plant are used for medicinal and
food preparation. The rhizome is an underground stem that is thick and
fleshy ringed with the bases of old leaves. Rhizomes are boiled and then
dried and ground to make the distinctive bright yellow spice, turmeric.
Turmeric History:
Probably
originating from India, turmeric has been used in India for at least
2500 years. It is most common in southern Asia and particularly in
India. Turmeric was probably cultivated at first as a dye and later on
it was used as cosmetic and as an auspicious and aromatic food
substance. It possesses antiseptic, anti-inflammatory detoxifying
properties as well as carminative properties. Turmeric has a long
history of medicinal use in South Asia and was widely used in Ayurvedic,
Siddha and Unani systems. It is thought to be a hybrid selection and
vegetative propagation of wild turmeric (Curcuma aromatica), which is
native to India, Sri Lanka and the eastern Himalayas and some other
closely related species.
Curcumin and Alzheimer's Disease
Worldwide, there are over 1000 published animal and human studies, both in vivo and in vitro
in which the effects of curcumin on various diseases have been
examined. Studies include epidemiological, basic and clinical research
on AD.
Bio Chemical properties
Epidemiological Studies
Various studies and research[
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results indicate a lower incidence and prevalence of AD in India. The
prevalence of AD among adults aged 70-79 years in India is 4.4 times
less than that of adults aged 70-79 years in the United States.[
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Researchers investigated the association between the curry consumption
and cognitive level in 1010 Asians between 60 and 93 years of age. The
study found that those who occasionally ate curry (less than once a
month) and often (more than once a month) performed better on a standard
test (MMSE) of cognitive function than those who ate curry never or
rarely.[
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Destroy user interface control10]Mechanism of action of curcumin on Alzheimer's disease:
The
process through which AD degrades the nerve cells is believed to
involve certain properties: inflammation, oxidative damage and most
notably, the formation of beta-amyloid plaques, metal toxicity [Figure 3]. There have been several studies on effects of curcumin on AD. Outlined below are some of the studies and their conclusions.
Different mechanisms of action of curcumin in AD
Effects of Curcumin on Macrophages
A
study conducted at UCLA found that curcumin may help the macrophages to
clear the amyloid plaques found in Alzheimer's disease. Macrophages
play an important role in the immune system. They help the body to fight
against foreign proteins and then effectively clear them. Curcumin was
treated with macrophages in blood taken from nine volunteers: six AD
patients and three healthy controls. Beta amyloid was then introduced.
The AD patients, whose macrophages were treated with curcumin, when
compared with patients whose macrophages were not treated with curcumin,
showed an improved uptake and ingestion of the plaques. Thus, curcumin
may support the immune system to clear the amyloid protein.[
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Destroy user interface control11]Curcumin on glial cells:
Recent
histological studies reveal the presence of activated microglia and
reactive astrocytes around A-beta plaques in brains from patients with
AD. The chronic activation of microglia secretes cytokines and some
reactive substances that exacerbate A-beta pathology. So neuroglia is an
important part in the pathogenesis of AD. Curcumin has a lipophilic
property and can pass through all cell membranes and thus exerts its
intracellular effects. Curcumin has anti-proliferative actions on
microglia. A minimal dose of curcumin affects neuroglial proliferation
and differentiation. Its inhibition of microglial proliferation and
differentiation were studied and researched by the University of
Southern California Los Angeles (UCLA). Researchers[
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using doses of 4, 5, 10, 15, 20 microM concentration of curcumin in C-6
rat glioma 2B-clone cells, a mixed colony of both neuroglial cells in a
six- day trial, showed that curcumin dose dependently stops the
proliferation of neuroglial cells, by differentiate into a mature cell
or undergo apoptosis. It inhibits neuroglial cells proliferation dose
dependently (i.e.) higher the concentration, the greater the inhibition.
It has shown to decrease the glutamine synthetase (GS) assay, a marker
enzyme for astrocytes. In the same study, curcumin was shown to increase
CNP (2′3′- cyclic Nucleotide 3′-phosphohydrolase), a marker enzyme for
oligodendrocytes. The overall effect of curcumin on neuroglial cells
involves decreased astrocytes proliferation, improved myelogenesis and
increased activity and differentiation of oligodendrocytes.Curcumin as an Anti Inflammatory in Alzheimer's
One
of the important pathogenesis in Alzheimer's disease is the chronic
inflammation of nerve cells. Several studies have demonstrated the
associated inflammatory changes such as microgliosis, astrocytosis and
the presence of pro-inflammatory substances that accompany the
deposition of amyloid-β (Aβ) peptide. Patients with the prolonged use of
certain nonsteroidal anti-inflammatory (NSAID) drugs such as ibuprofen
have been shown to have a reduced risk of developing the symptoms of AD;
however, the chronic use of NSAID can cause a toxic effect on the
kidneys, liver and GI track. Curcumin has a potent anti-inflammatory
effect. Through its various anti-inflammatory effects, it may have a
role in the cure of AD. Curcumin inhibits Aβ-induced expression of Egr-1
protein and Egr-1 DNA-binding activity in THP-1 monocytic cells.
Studies have shown the role of Egr-1 in amyloid peptide-induced
cytochemokine gene expression in monocytes. By inhibition of Egr-1
DNA-binding activity by curcumin, it reduces the inflammation. The
chemotaxis of monocytes, which can occur in response to chemokines from
activated microglia and astrocytes in the brain, can be decreased by
curcumin.[
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Curcumin
is found to inhibit cyclooxygenase (COX-2), phospholipases,
transcription factor and enzymes involved in metabolizing the membrane
phospholipids into prostaglandins. The reduction of the release of ROS
by stimulated neutrophils, inhibition of AP-1 and NF-Kappa B inhibit the
activation of the pro-inflammatory cytokines TNF (tumor necrosis
factor)-alpha and IL (interleukin)-1 beta.[
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Overall, curcumin decreases the main chemical for inflammation and the
transcription of inflammatory cytokines. Curcumin inhibits intracellular
IL-12 p40/p70 and IL-12 p70 expression. The exposure to curcumin also
impaired the production of pro-inflammatory cytokines (IL-1, IL-6 and
TNF-). These studies indicate a potent inhibitor of pro-inflammatory
cytokine production by curcumin and it may differ according to the
nature of the target cells.Curcumin as an Anti-oxidant
Curcumin
inhibits the activity of AP-1, a transcription factor involved in
expression of amyloid, which is linked to AD. Curcuminoids are proven to
have strong antioxidant action demonstrated by the inhibition of the
formation and propagation of free radicals. It decreases the low-density
lipoprotein oxidation and the free radicals that cause the
deterioration of neurons, not only in AD but also in other neuron
degenerative disorders such as Huntington's and Parkinson's disease.[
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In one study, curcuma oil (500 mg Kg(-1) i.p.) was given 15 min before 2
h middle cerebral artery occlusion, followed by 24 h reflow in rats.
This significantly diminished the infarct volume, improved neurological
deficit and counteracted oxidative stress.[
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A
study conducted at Nanjing Medical University (China) showed that a
single injection of curcumin (1 and 2 mg/kg, i.v.) after focal cerebral
ischemia/reperfusion in rats significantly diminished the infarct
volume, improved neurological deficit, decreased mortality and reduced
the water content in the brain.[
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Curcumin
has powerful antioxidant and anti-inflammatory properties; according to
the scientists, these properties believe help ease Alzheimer's symptoms
caused by oxidation and inflammation.[
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A study conducted at Jawaharlal Nehru University (India) demonstrated
that the administration of curcumin significantly reduced lipid
peroxidation and lipofuscin accumulation that is normally increased with
aging.[
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It also increased the activity of superoxide dismutase,
sodium-potassium ATPase that normally decreased with aging. In another
study, curcumin has been shown to protect the cells from betaA (1-42)
insult through antioxidant pathway.[
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Curcumin protects brain mitochondria against various oxidative stress.
Pre-treatment with curcumin protects brain mitochondria against
peroxynitrite (a product of the reaction of nitric oxide with
superoxide) a potent and versatile oxidant that can attack a wide range
of cells in vitro by direct detoxification and in vivo by the elevation of total cellular glutathione levels.[
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Natural
antioxidant curcumin has been identified as a potent inducer of
hemoxygenase, a protein that provides efficient cytoprotection against
various forms of oxidative stress. By promoting the inactivation of
Nrf2-keap1 complex and increased binding to no-1ARE, curcumin induces
hemoxygenase activity. The incubation of astrocytes with curcumin at a
concentration that promoted hemoxygenase activity resulted in an early
increase in reduced glutathione, followed by a significant elevation in
oxidized glutathione content.[
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Glutathione is an important water-phase antioxidant and essential
cofactor for antioxidant enzymes protecting the mitochondria against
endogenous oxygen radicals. Its level reflects the free radical
scavenging capacity of the body. GSH depletion leads to tissue damage
due to lipid peroxidation and oxidative damage.Beta-Amyloid Plaques
The
most prominent characteristic feature in AD is the presence of
beta-amyloid plaques. These plaques are basically an accumulation of
small fibers called beta amyloid fibrils. Because the deposition of
beta-amyloid protein is a consistent pathological hallmark of brains
affected by AD, the inhibition of A-beta generation, prevention of
A-beta fibril formation, destabilization of pre-formed A-beta would be
an attractive therapeutic strategy for the treatment of AD. The levels
of beta-amyloid in AD mice that were given low doses of curcumin were
decreased by around 40% in comparison to those that were not treated
with curcumin. In addition, low doses of curcumin also caused a 43%
decrease in the so-called “plaque burden” that these beta-amyloid have
on the brains of AD mice. Surprisingly low doses of curcumin given over
longer period were actually more effective than high doses in combating
the neurodegenerative process of AD.[
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At higher concentration, curcumin binds to amyloid beta and blocks its
self assembly. The key chemical features in amyloid beta are the
presence of two aromatic end groups and any alterations in these groups
has profound effect on its activity.
Because of the
lipophilic nature of curcumin, it crosses the blood brain barrier and
binds to plaques. Curcumin was a better A-beta 40 aggregation inhibitor
and it destabilizes the A-beta polymer. In in vitro studies,
curcumin inhibits aggregation as well as disaggregates to form fibrillar
A-beta 40. A Japanese study showed that using fluorescence
spectroscopic analysis with thioflavin T and electron microscopic
studies, curcumin destabilizes the fA-beta(1-40) and fA-beta(1-42) as
well as their extension.[
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Curcumin-derived isoxazoles and pyrazoles bind to the amyloid beta
peptide (Abeta) and inhibit amyloid precursor protein (APP) metabolism.[
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Curcumin given to APPswe/PS1dE9 mice for 7 days crosses the blood-brain
barrier as demonstrated by muliti-photon microscopy and reduces the
existing senile plaques.[
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In another study, curcumin has been shown to increase the phagocytosis
of amyloid-beta, effectively clearing them from the brains of patients
with AD.[
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Studies
showed that metals can induce A-beta aggregation and toxicity and are
concentrated on Alzheimer's brain. Chelators' desferroxamine and
cliquinol have exhibited anti-Alzheimer's effects. A study at Capital
University Beijing demonstrated the toxicity of copper on neurons. A
greater amount of H2O2 was released when copper
(2)-A(beta)-40 complexes were added to the xanthene oxidase system.
Copper was bound to A(beta)1-40 and was observed by electron
paramagnetic resonance spectroscopy. In addition, copper chelators could
cause a structural transition of A(beta). There was an increase on beta
sheet as well as alpha-helix when copper was introduced.[
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Another study reveals that copper and zinc bind A-beta inducing
aggregation and give rise to reactive oxygen species. There was a
conformational change from beta sheet to alpha helix followed by peptide
oligomerization and membrane penetration, when copper (or) zinc is
added to A-beta in a negatively charged lipid environment.[
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Brain iron deregulation and its association with amyloid precursor
protein plaque formation are implicated in the pathology of AD.[
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Curcumin,
by interaction with heavy metals such as cadmium and lead, prevents
neurotoxicity caused by these metals. The intraperitoneal injection of
lead acetate in rats in the presence of curcumin was studied
microscopically. The results show lead-induced damage to neurons was
significantly reduced in rats injected with curcumin.[
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A study at Chinese University of Hong Kong showed that by using
spectrophotometry, the curcumin effectively binds to copper, zinc and
iron. In addition, curcumin binds more effectively with redox-active
metals such as iron and copper than the redox-inactive zinc. It is
suggested that curcumin suppresses inflammatory damage by preventing
metal induction of NF-kappa.[
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High-fat
diets and increased blood cholesterol are linked to increased amyloid
plaques by the intracellular accumulation of cholestryl esters.[
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Researchers believe that by inhibiting cholesterol formation and
decreasing serum peroxides, curcumin might exert beneficial effects on
AD.[
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Oral bioavailability:
Curcumin
has poor bioavailability. Because curcumin readily conjugated in the
intestine and liver to form curcumin glucuronides.[
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In a clinical trial conducted in Taiwan, serum curcumin concentrations
peaked one to two hours after an oral dose. Peak serum concentrations
were 0.5, 0.6 and 1.8 micromoles/L at doses of 4, 6 and 8 g/day
respectively.[
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It is also measured in urine at a dose of 3.6 g/day. Absorption is poor
following ingestion in mice and rats. 38% to 75% of an ingested dose of
curcumin is excreted in the feces. Absorption appears to be better with
food. Curcumin crosses the blood brain barrier and is detected in CSF.Side Effect
No
apparent side effects have been reported thus far. GI upset, chest
tightness, skin rashes, swollen skin are said to occur with high dose. A
few cases of allergic contact dermatitis from curcumin have been
reported.[
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The
chronic use of curcumin can cause liver toxicity. For this reason,
turmeric products should probably be avoided by individuals with liver
disease, heavy drinkers and those who take prescription medications that
are metabolized by liver. Curcumin was found to be pharmacologically
safe in human clinical trials with doses up to 10 g/day. A phase 1 human
trial with 25 subjects using up to 8000 mg of curcumin per day for
three months found no toxicity from curcumin.[
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Curcumin
is said to interact with certain drugs such as blood thinning agents,
NSAIDs, reserpin. Co-supplementation with 20 mg of piperine (extracted
from black pepper) significantly increase the bioavailablity of curcumin
by 2000%.[
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Curcumin
is not recommended for persons with biliary tract obstruction because
it stimulates bile secretion. It is also not recommended for people with
gallstones, obstructive jaundice and acute biliary colic. Curcumin
supplementation of 20-40 mg have been reported to increase gallbladder
contractions in healthy people.[
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Epidemiological
studies have shown that prevalence of AD is 4.4 lower amongst Indian
Asians as compared to people of western origin.[
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Destroy user interface control9] D ementia incidence in western countries (P < 0.21) and East Asian countries were lower than that of Europe (P < 0.0004).[
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Experimental studies: Statistical significance
Clinical -Vivo:
Blood from six patients with AD and three healthy controls was taken
and the macrophage cells were isolated. After treatment of macrophages
with curcuminoids, Aβ uptake by macrophages of three of the six AD
patients was found to have significantly increased (P < 0.001 to 0.081).[
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Five animal and two human studies showed statistically significant P values.
Conclusion
Based
on the main findings detailed above, curcumin will lead to a promising
treatment for Alzheimer's disease. The clinically studied chemical
properties of curcumin and its various effects on AD shows the
possibility to do further research and develop better drugs based on
curcumin for treating AD. The recent review paper of John Ringman also
supports some of the abovementioned properties of curcumin in AD;[
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Several
unanswered questions remain: What is the one main chemical property of
curcumin that can be exploited in treating AD? What is the role of
curcumin in other neurological disorders such as Parkinson's,
Huntington's and other dementias? How does curcumin interact with
neuronal plaques? Is it effective only as a food additive? Would it be
effective when used alone or with other anti inflammatory drugs?
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