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DOI: 10.1201/9781003300502-11
11
Plant Phenols and Their
Potential Modulation
of Neurochemistry
Rahul Kumar Sharma, Shilpa Thakur, Navidha Aggarwal,
and Hitesh Chopra
11.1 INTRODUCTION
Flora and fauna are the gifts of nature. Many plants have been used to treat many ailments for many
decades. The plants have a pharmacologically active substance that is responsible for many bio-
logical activities [1– 3]. They are alkaloids, terpenoids, phenols and phenolic glycosides, coumarins
heterosides, mucilage and gums, tannins, volatile oils, saponins, cardioactive glycosides, cyano-
genic glycosides, etc. The majority of plants’ secondary metabolites are polyphenols, also referred
to as polyhydroxyphenols. They are part of a structural class of organic compounds that are
distinguished by the presence of many phenols’ structural units. The distinct physical, chemical,
and biological (metabolic, poisonous, medicinal, etc.) characteristics of certain members of the
class are a result of these phenol structures. Its chemical structure, produced by joining an aromatic
phenyl ring to a hydroxyl (- OH) group, is known as phenol. The majority of fruits, vegetables,
cereals, and beverages contain polyphenols, which are naturally occurring chemicals. Up to 200–
300 mg of polyphenols is present in every 100 g of dry mass of fruits like berries, grapes, apples,
pears, cherries [4]. Quercetin and catechin are two instances of free monomers of polyphenols that
can be present in food, along with oligomers (procyanidins). They often exist as free aglycones
or are associated with saccharides as glycosides [5]. Strong evidence came from epidemiological
studies and related meta- analyses suggesting long- term intake of diets high in plant polyphenols
provides some protection against the onset of malignancies, cardiovascular illnesses, diabetes,
osteoporosis, and neurological diseases [6– 13
in the pathophysiology of these diseases, in addition to other variables. Flavonoids exhibit a sig-
14– 18]. In vitro, polyphenols
exert powerful antioxidant effects via a variety of mechanisms, including radical scavenging, che-
lation of metal ions (Fe, Cu, and others), and regulation of antioxidant enzyme activity. By giving a
hydrogen atom from their hydroxyl groups to radicals, phenolic - OH groups’ position and number
affect their capability to scavenge, which leads to the removal of radical moiety. The phenoxy
radical that can produce stable compounds and end radical reactions by reacting with another
radical is created during this reaction.
When consumed in food, polyphenols are present as esters, glycosides, or polymers that the
intestines are unable to absorb. The native polyphenolic chemical molecules are digested by micro-
bial enzymes in the colon, changed to derivatives by methylation, sulfation, and glucuronidation,
and then absorbed in the colon and transported through the blood to numerous tissues and organs,
including the brain. Moreover, the bioavailability of phenolic substances can range from extremely
227
Plant Phenols and Their Potential Modulation of Neurochemistry
low to incredibly high due to their various susceptibilities to colon enzyme metabolism [19,20]. In
comparison to other low- molecular- weight antioxidants like vitamins C and E and uric acid, poly-
phenolic substances have lower direct antioxidant action because of their low bioavailability and in
vivo conversion to various derivatives.
the fate of cells [21,22
opment, or death. The neuroprotective properties of polyphenols are responsible for the stimulation
of NO production in the endothelium and the suppression of platelet aggregation, both of which
Polyphenols might modify brain function at three locations:
(i)
signalling pathways that connect the brain to peripheral organs.
(ii)
including multi- drug resistance proteins.
(iii) Within the CNS, via altering the activity of neurons and glial cells.
The neuroprotective effects of polyphenols, in addition to their antioxidant properties, have been
demonstrated to be mediated by modulation of cellular signalling pathways involved in cognitive
processes like synaptic plasticity, particularly those that involve CREB (cAMP- response element-
binding protein) signalling. This transcription factor, known as CREB, is connected to genes
that express brain- derived neurotrophic factor (BDNF). Many researchers suggested that CREB
activity can affect memory development and, conversely, that higher CREB activity can accel-
erate memory formation, highlighting the crucial role that CREB plays in brain function [23,24].
By activating BDNF after inducing CREB, polyphenols can potentially modify these signalling
pathways [25].
11.2 POLYPHENOLSSTRUCTURE AND CLASSIFICATION
More than 8,000 polyphenolic chemical compounds can be found in a variety of plant species. All
plant phenolic compounds begin with phenylalanine or a nearby precursor called shikimic acid.
Although sugar (polysaccharide or monosaccharide) and an aromatic carbon can also be linked dir-
ectly, they are most frequently found in conjugated forms with one or more sugar residues attached
to hydroxyl groups. Polyphenols can be categorised into different classes based on the number of
phenol rings they contain, as well as the structural elements that hold these rings together (See
Figure 11.1).
11.3 NEURODEGENERATIVE DISORDERS
Neurodegeneration is the term used to describe the gradual loss of a neuron’s structure and/ or
after birth, or it may even be caused by an injury [26,27]. There are thought to be a few hundred
different neurodegenerative disorders, and many of them appear to share clinical and pathological
characteristics. Longer life lengths are one of the greatest issues facing medical science, as
neurodegenerative illnesses are a major source of mortality and disability. Although the causes of
apoptosis, amyloid cascade, oxidative stress, and sodium nitrite- mediated neurodegeneration.
Superoxide, hydroxyl radicals, and hydrogen peroxide are examples of reactive oxygen species
(ROS) that are produced endogenously and play helpful roles in cellular processes. However, they
can take part in detrimental processes, including neurodegeneration. Neurodegenerative illnesses like
228
Plant-based Foods and their Implications in Brain Health
amyotrophic lateral sclerosis, Alzheimer’s, Huntington’s, and Parkinson’s diseases have received a
lot of attention, and it has been established that these illnesses are closely related to mitochondrial
malfunction brought on by ROS. Neuroprotection refers to any medical method, including drugs
and treatments, that stop neurons from dying. Limiting neuronal dysfunction following damage is
the aim of neuroprotection, which also aims to preserve the integrity of any cellular interactions
that might occur in the brain and preserve neural function. Antioxidants are useful in reducing or
avoiding certain illnesses because they neutralise free radicals[28– 30].
11.4 ROLE OF PLANT PHENOL ON NEUROCHEMISTRY
Plants have been used to treat a variety of human diseases since antiquity. India is one of the world’s
top 12 mega- diversity countries due to the large number of species there. Meanwhile, neurological
illnesses are frequently not regarded as common diseases, and many persons with psychological
disorders, like epilepsy, are profoundly impacted by stigma and discrimination connected to
health. The majority of the population relies on traditional medicine for basic health care. Others,
such as meningitis, stroke, Parkinson’s, and Alzheimer’s. Speaking, breathing, movement, mood,
and memory are all impacted by nervous system problems. The brain and spinal cord are impacted
by neurological conditions. By attaching to different receptors, polyphenols in cerebral tissue
(resveratrol and epigallocatechin gallate) and protein kinase C (PKC) pathways, phosphoinositide-
3- (PI3) kinase (curcumin), mitogen- activated protein (MAP) kinase, and phosphoinositide- 3-
memory, and the prevention of amyloid plaque formation. They can also affect cell survival (by
encouraging NO production in the endothelium and inhibiting platelet aggregation, polyphenols
31].
FIGURE 11.1 Types of Phenol.
229
Plant Phenols and Their Potential Modulation of Neurochemistry
(continued)
TABLE 11.1
Phenolic plant sources and their medicinal effects
Plant Family Chemicals Plant part Pharmacologically use References
Rauwola
serpentina
Apocyanaceae Ajmaline, ajmalicine,
reserpine, serpentine
Root Insomnia, mental
disorders, aggressive
behaviour,
schizophrenia,
epilepsy, psychosis
[32]
Aegle marmelos Rutaceae Carotenoids, tannic acid,
ageline, aegelenine,
mermelosinmarmesinin,
ascorbic acid, eugenol,
skimmianine and
saponin
Leaves Fatigue, anxiety,
depression
[33]
Rosmarinus
ofcinalis
Lamiaceae Rosemary diterpenes,
p- cymene, linalool,
eucalyptol, beta- pinene
Whole plant Depression, anxiety [34]
Withaniasomnifera Solanaceae Somniferinine,
withananine, Withanine,
somniferine, somnine
Roots, stems,
and leaves
Nervous disorders,
arthritis, rheumatism,
amnesia, insomnia,
stress and anxiety,
paralysis, Alzheimer's
disease
[35]
Bacopa monnieri Plantaginaceae Alkaloids, brahmine,
herpestine, saponins,
stigmasterols
Whole plant,
leaf
epilepsy, schizophrenia,
and dissociative
disorder
[36]
Datura metel Solanaceae Hyoscyamine,
norhyoscyamine,
norscopolamine
Leaf, seed Increase the heart rate,
induce relaxation
and motor inhibition
in smooth muscles,
decrease secretions
and induce dilation of
the pupils of the eyes.
Rheumatism
[37]
Centella asiatica Apiaceae Triterpenoids, volatile
fatty acids, glycosides,
and tannins,
Whole plant,
leaf, stem
psychosis, epilepsy and
insomnia, mental
disorders, memory
[38]
Ginkgo biloba Ginkgoaceae Trilactonic diterpenes
(ginkgolide A- C,
ginkgolide J- M),
trilactonic sesquiterpene
(Bilobalide), and
Leaf Alzheimer’s disease [39]
Turmeric Zingiberaceae Curcumin, curcuminoids,
turmerones, sabinene,
cineol
Rhizome Alzheimer’s disease,
arthritis, bone
fracture, depression,
hypertension
[40]
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Plant-based Foods and their Implications in Brain Health
11.5 ROLE OF PLANT PHENOLS IN NEURODEGENERATIVE
DISORDERS
Mental health issues in children, adolescents, and adults are usually caused by neurodegenerative
describes a condition in which the production of free radicals and/ or reactive oxygen species/ reactive
nitrogen species (ROS/ RNS) outweighs the antioxidant defence, favouring ROS/ RNS, resulting in
oxidative damage to lipids, proteins, and DNA, and eventually cell and organ dysfunction. The brain
is a lipid- rich organ, which can contribute to its susceptibility to oxidative damage. Compared to
other organs of the body, the CNS’s cells are more vulnerable to ROS’ harmful effects. Additionally,
compared to other cells, the brain has lower levels of catalase, glutathione peroxidase, and super-
oxide dismutase (enzymes that break down hydrogen peroxide or organic peroxides), as well as a
higher concentration of iron ions and ascorbic acid, which together create the ideal environment for
the formation of the extremely toxic hydroxyl radical. The brain is more vulnerable to oxidative and
peroxidative damage to biomolecules as a result of these facts. By altering particular cellular signal-
ling pathways involved in cognitive processes like synaptic plasticity, polyphenols can exhibit their
neuroprotective effects. Polyphenols can directly modulate these signalling pathways by induction
of CREB [47].
Plant Family Chemicals Plant part Pharmacologically use References
Embilica
ofcinalis
Euphorbiaceae Gallic acid, catechol,
ascorbic acid, ellagic
acid, rutin, quercetin
Fruit memory loss, mental
fatigue, anxiety,
depression,
migraine, insomnia,
hyperactivity disorder
[41]
Acorus calamus Acoraceae
isoeugenol, camphor,
calamol, azulene
Whole plant,
rhizome
Epilepsy, mental
problems, psychosis,
dissociative disorder
[42]
Terminalia
chebula
Combretaceae chebulinic acid, chebulic
acid, gallic acid,
coumarin, punicalagin,
corilagin, ellagic acid,
chebulagic acid
Fruit Schizophrenia and
mental retardation
[43]
Panax Ginseng Araliaceae Ginsenoside Root Parkinson’s disease,
Alzheimer's disease,
cancer, antianxiety,
antidepressant,
hypertension and
diabetes
[44]
Cassia stula Fabaceae
proanthocyanides,
polyphenol, terpenoids
Leaves, fruit anti- tumour,
antidepressant,
anxiety, antidiabetic,
paralysis, rheumatism
and gout
[45]
Zingiber ofcinale Zingiberaceae Gingerols, shogaols Rhizome Rheumatism, migraine,
muscular strength,
schizophrenia
[46]
TABLE 11.1 (Continued)
Phenolic plant sources and their medicinal effects
231
Plant Phenols and Their Potential Modulation of Neurochemistry
11.5.1 alzheimer’S diSeaSe
Alzheimer’s disease (AD) is a prevalent form of dementia that is caused by ageing as opposed to
plaques are all symptoms of AD (particularly cholinergic neurons of the basal forebrain) [48– 50].
These anatomical defects can be seen in the brains of AD patients. Loss of neurons that release acetyl-
pallidus. The dispersion of these neurons’ axons, which are characteristic of Alzheimer’s disease,
is widespread across the limbic and cerebral cortex. β- Amyloid plaques, aberrant protein clusters
of neurons in affected brain regions. This tau protein, which has undergone hyperphosphorylation,
-
depletion, and, ultimately, cell death. The loss of cortical and subcortical neurons and severe atrophy
of the cerebral cortex are hallmarks of AD. Numerous neuronal systems employ glutamate as a
neurotransmitter, and it is thought that glutamate mediates the majority of excitatory synaptic trans-
mission in mammalian brains. Even while glutamate is necessary for healthy brain function, too
much of it can cause excitotoxicity, which is the death of cells [51]. Glutamate receptors, especially
those of the N- Methyl- D- Aspartate (NMDA) type, mediate the damaging effects of glutamate. The
complicated character of polyphenols with regard to their bioactivity and bioavailability in the brain
hinders their progression in the treatment of neurological problems. Dietary intake of polyphenols
has been designed to improve cognitive abilities while lowering free radical controlling signalling
pathways and reducing the risk of AD.
-
logical process [52]. The predominance of curcumin’s chemical makeup makes it a lipophilic sub-
stance that easily crosses the blood- brain barrier, forms plaques, and inhibits the amyloid peptide’s
aggregation and disaggregation models. Increasing evidence indicates that the PI3K/ Akt/ GSK- 3
53,54].
11.5.2 parkinSon’S diSeaSe
Parkinson’s disease is a progressive, age- related movement disorder whose neuropathology
is characterized by deterioration of the afferent pigmented neurons of the substantia nigra [55].
Dopaminergic neurons in the substantia nigra pars compacta deteriorate as a result of the motor
and cognitive impairment that underlies PD (SNpc). Due to the persistent accumulation of pro-
tein inclusions containing ubiquitin in the cytoplasm of the chosen neuron, which results in their
death, trademark lesions known as Lewy bodies are produced [56,57]. Tremor, stiffness, slowness,
depression, and dementia are a few subsequent symptoms.
In a rat model of PD, resveratrol has been demonstrated to lessen oxidative stress, lipid
peroxidation, and protein carbonyl (PC), as well as to decrease cyclooxygenase- 2 (COX- 2) and
TNF- alpha encoded mRNA levels in the substantia nigra [58]. Oxyresveratrol has been shown
to lessen brain damage in SH- SY5Y cells by increasing SIRT1 levels and decreasing the expres-
sion of caspase- 3, c- Jun N- terminal kinase (JNK), and c- Jun transcription factors. Similar to oxy-
resveratrol, ferulic acid has shown that inhibiting the JNK pathway has neuroprotective effects [59].
11.5.3 huntington’S diSeaSe
Huntington’s disease (HD) is a hereditary (autosomal dominant) disorder characterised by pro-
gressive brain deterioration that begins in adulthood and progresses quickly till death [60– 62].
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Plant-based Foods and their Implications in Brain Health
HD’s foundation is made up of the enlarged polyglutamine region of the huntingtin protein and
the AG triplet nucleotide repetitions. It results in severe motor symptoms such as uncontrollable
writhing motions, which are quite incapacitating. Balance is hampered, movements become more
pronounced, and dysarthria and dysphasia start to occur. The striatum (caudate/ putamen) of the brain
these structures, which then affects the anterior region from the mediodorsal to the ventrolateral.
The emergence of chorea, the most obvious clinical symptom of HD, also appears to be mediated
by selective vulnerability. The typical age of onset is between 35 and 40 years old, but the age
ranges from 2 years old to the middle of one’s 80s. Even though both parents contribute equally
to the defect’s inheritance, the father accounts for more than 80% of cases when symptoms appear
before age 20. Particularly if one parent possesses an intermediate gene, the disease can develop in
unaffected parents.
1alpha (peroxisome proliferative activated receptor, gamma) signalling pathway [63]. Hesperidin
and naringenin, abundant in citrus fruits, induced neuroprotection in rats, possibly via nitric oxide
synthase (NOS) inhibition [64]. Curcumin has been demonstrated to alter a number of transgene-
dependent metrics and reduce Huntington aggregates, suggesting a potential therapeutic effect
in HD [65]. According to the available preclinical evidence, polyphenols provide substantial
neuroprotection through genetic and immunological regulation, offering hope for the clinical delay
or prevention of neurological illnesses like PD and HD.
the United States, which is brought on by an abrupt obstruction of the CNS’s blood supply. They
-
lateral circulation if an obstruction develops within or close to the cerebral arterial circle. When a
thrombotic event occurs, the blood vessel that supplies blood to the brain becomes dysfunctional
Neuroprotective activity by down regulation of the matrix metalloproteinase (MMP) in the mice
model of the cerebral ischaemia has been exhibited by green tea polyphenol, EGCG [66]. Green tea
polyphenols have been discovered to play a role in the defence of neurons against hypoxia- induced
degeneration [67]. To attenuate ischaemic injury, quercetin played a crucial role by controlling the
peroxidation of lipids in neurons and the acid- sensing of ion channels that led to dysregulation [68].
Quercetin has decreased blood- brain barrier interruption and lowered MMP- 9 levels in tests of cere-
bral ischaemia by using the same antioxidant analyses as green tea polyphenols [69].
Serotonin abnormalities, abnormal serotonin receptors, and depression are thought to be causally
related, but dopamine, adrenaline, and glutamate are also thought to play a role [70,71]. Enzymes
involved in the breakdown of neurotransmitters, such as monoamine oxidase (MAO), and the syn-
thesis of their amino acid precursor tryptophan by the enzyme tryptophan hydroxylase both affect
neurotransmitter metabolism [72
depressed people when their blood levels of these cytokines are elevated. These reliable markers of
as well as several co- morbid conditions like fatigue, poor sleep, and cognitive impairment [73,74].
When curcumin and the alkaloid piperine were taken together, MAO activity was inhibited, and
levels of serotonin and dopamine were raised [75]. It is thought that curcumin’s ability to inhibit lipid
peroxidation and neutralise ROS and RNS is what allows it to easily cross the blood- brain barrier
and induce neuroprotection [76,77
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Plant Phenols and Their Potential Modulation of Neurochemistry
and antioxidant activities as well as its capacity to reduce stress and depression. In a mouse study,
higher levels of BDNF or lower levels of serum corticosterone and adrenocorticotropic hormone
were found in response to long- term administration of green tea polyphenols or a forced swimming
test, respectively [78].
Schizophrenia is a severe mental illness that manifests as distorted behaviour and abnormal
thinking processes. Psychological and social processes, as well as genetic and early environmental
primarily affects thinking, it frequently exacerbates long- term issues with behaviour and emotions.
The pathophysiology of schizophrenia is thought to be related to increased oxidative stress [79].
The brain has a very high metabolic rate of oxidation. The brain’s high concentrations of the
neurotransmitters dopamine, adrenaline, and noradrenaline can also cause auto- oxidation, which
radical can also be overproduced by neuronal mitochondria. Mitochondria become harmed and dys-
-
thione (GSH), the main free radical scavenger in the brain [80]. In the prefrontal cortex of rodents
and humans, glutathione and redox regulation play a crucial role in myelination processes and white
matter maturation, a mechanism that may be compromised in schizophrenia.
epigallocatechin- 3- gallate (EGCG) [81
shown in an ex vivo study to lessen the lipid peroxidation caused by haloperidol in human plasma
[82]. The blood- brain barrier is crossed by EGb- 761, a Ginkgo biloba extract that shields the brain
from the harmful effects of oxidative stress due to its predominantly lipophilic components [83].
11.6 CONCLUSION
of memory, learning, and cognitive abilities. Despite the fact that many of the mechanisms under-
Protective against age- related diseases, dietary polyphenols are overwhelmingly chemically reactive,
with the vast majority being electrophilic. Because of their unique chemical composition, these
-
ively). However, much of the information we have on their bioactivity comes from in vitro or in vivo
research that lasted just a few weeks and employed doses that were not relevant to human nutrition.
It is still unclear how much polyphenol effects contribute in vivo and at physiologically relevant
concentrations to the advantages of consuming a diet rich in fruits and vegetables, despite the fact
that the weight of evidence suggests that they do. Whether or if this class of chemicals is associated
with health advantages has to be shown, as does the positive impact these compounds have on slowly
progressing neurodegenerative illnesses. The intake of polyphenol- rich foods throughout life has the
potential to limit neurodegeneration and prevent or repair age- dependent deteriorations in cognitive
function due to their various biological activities. However, clinical translation of the therapeutic
and pharmacological potential of these natural chemicals is still lacking. In addition, random clinical
trial effectiveness is required to back up the generally consistent epidemiological and mechanistic
absorption and metabolism of different polyphenols in humans have shown that the majority of
polyphenols share common pathways for their metabolism, most notably via their bacterial metab-
olism in the large intestine. Therefore, studies of smaller polar polyphenols for brain bioavailability