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Plant-based Foods and their Implications in Brain Health
catechin, accounting for approximately 50% – 80% of the total catechin concentration [89, 90].
suggestions that it has the capacity to mitigate memory impairment and neurodegeneration in
dementia [91]. Guo et al. [92] also examined the effectiveness of oral administration of ECCG in
mitigating AD- related memory impairment. In the study using the senescence- accelerated mouse
prone 8 AD model, it was observed that long- term oral administration of EGCG ameliorated spa-
tial learning and memory impairments and rescued the reduction in synaptic proteins observed in
the AD mouse model [92]. Also, in mice with anaesthesia- induced memory impairments, ECCG
93].
ECCG has also been shown to mitigate short- term memory loss in Williams- Beuren syndrome [87].
Berberine is another polyphenolic compound with reported nootropic properties. Berberine is an
isoquinoline alkaloid that has been isolated from Rhizoma coptidis (a Chinese herb with traditional
medicinal value, particularly in the management of memory impairment) or Berberis sibirica [94–
96
spatial learning capacity and memory retention and the attenuation of tau hyperphosphorylation via
94, 95].
Szalak et al. [97] also observed that chronic administration of berberine at 5 mg/ kg body weight
improved long- term memory acquisition in mice and increased the concentration of parvalbumin-
98]. Ginkgolides are biologically
active diterpenoids found in Ginkgo biloba. A number of these terpene lactones have been isolated,
although ginkgolide B is the most abundant bioactive constituent of the Ginkgo biloba extract [99].
The nootropic effects of ginkgolide B and K have also been reported [99, 100]. Huang et al. [99]
examined the effects of ginkgolide B in a rodent model of vascular dementia and observed that
100] examined the
effects of ginkgolide K on memory function in APP/ PS1 mice and observed that ginkgolide K
reversed memory impairment and downregulated the expression of mitochondrial calcium (Ca
2+
)
uniporter in the brain of these mice. Bilobalide is another bioactive constituent of gingko biloba
leaves, which has documented nootropic effects [101, 102]. The results of two different studies
that evaluated the effects of bilobalide on cognition in a mouse model of AD [101] and a mouse
model of vascular dementia [102] observed that bilobalide protected against the development of
102]. In rats
101]. Ginsenosides are a group of
steroid glycosides and triterpene saponin, which are the main bioactive constituents of the Panax
ginseng plant. The ginsenosides are largely believed to be responsible for the memory- enhancing
effects of Panax ginseng [103]. A number of studies have reported the nootropic effects of different
forms of ginsenosides [103]. Kim et al. [103] observed that ginsenosides Rg5 or Rh3 reversed the
scopolamine- induced decrease in latency time in the passive avoidance test, increased spontan-
eous alteration in the Y- maze task, and shortened escape latencies in the Morris water maze. The
effects on memory were attributed to its ability to decrease acetylcholinesterase activity, modu-
late the expression of hippocampal brain- derived neurotrophic factor and the activation of cAMP
response element- binding protein [103]. Hou et al. [104] also reported that long- term administration
of ginsenoside Rh1 enhanced learning and memory in the passive avoidance test and Morris water
maze through the enhancement of hippocampal dentate gyrus cell survival and the upregulation of
brain- derived neurotrophic factor expression [104
25- 35
-
105]; they observed that ginsenoside
105
Herbs with Nootropic Efficacy
Bax, attenuate the cleavage of caspase- 3, and enhance the phosphorylation of Akt [105].
Although the nootropic abilities and neuroprotective effects of a number of these bioactive
compounds have been documented, their low bioavailability and limited transport ability across
the blood- brain barrier are among the drawbacks of their use [106, 107]. In the last few years,
there has been increasing awareness regarding the use of polymeric nanoparticles and liposomes to
improve the bioavailability of a number of these bioactive constituents [108]. They have also been
with receptors indirectly to enhance delivery across the blood- brain barrier [107, 108]. While there
compounds, bioactive constituents like curcumin and ginsenosides have been researched with
promising results [109, 110]. Maiti et al. [110] examined the effects of solid lipid curcumin particles
(SLCP) in one- year- old 5xFAD- and age- matched wild- type mice. The results showed that the
acute daily intraperitoneal injection of SLCP was associated with improved permeability and better
neuroprotective effect, suggesting that this could also enhance cognitive function. Hoppe et al [79]
examined the effects of acute intraperitoneal injection of curcumin- loaded lipid- core nanocapsules
79]. In
-
tration of curcumin and was associated with enhanced cognition and reduced oxidative stress in the
hippocampal tissue [80].
5.5 CONCLUSION
Nootropic herbs and herbal products research and applications have come some way in recent years,
modes of action. It is also noteworthy to acknowledge the fact that it is possible that herbal nootropics
may soon take centre stage in the management or possible prevention of human cognitive disorders.
While challenges relating to delivery to target tissues are now being tackled, we still have a long way to
go in this aspect. However, it brings a great sense of relief to know that a number of the answers we des-
perately seek have always been with us, and all we need to do is face the right direction for this.
TERMS AND ABBREVIATIONS
Aβ
AD Alzheimer’s disease
Akt protein kinase B
APP/PSI mice mouse/human amyloid precursor protein and a mutant human presenilin 1 mouse
Bcl-2 B cell lymphoma protein 2 family
Bax Bcl-2-associated X protein
cAMP cyclic adenosine monophosphate
ECCG epigallocatechin- 3- gallate
PKC protein kinase C
PI3K phosphatidylinositol 3- kinase
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DOI: 10.1201/9781003300502-6
6
Neuroprotective Potential of
Some Traditional Indian
Medicinal Plants in
Alzheimer’s and Parkinson’s
Disease
Bharti Chaudhry
6.1 INTRODUCTION
but also families and societies. Neurodegenerative diseases constitute a group of chronic, pro-
gressive disorders, characterized by progressive loss of neurons in discrete areas of the central
CNS region.
1
The disorders of the nervous system, including Alzheimer’s disease, Parkinson’s dis-
ease, amyotrophic lateral sclerosis, multiple sclerosis and Huntington’s disease, usually manifest
in cognitive decline, dementia, movement dysfunction, and changes in personality and behaviour.
Cognitive decline and senile dementia are emerging as serious global health concerns. As per the
WHO Global Status Report on the public health response to dementia, September 2021 (www.who.
int/ publi cati ons- det ail- redir ect/ 978924 0033 245), an estimated 55.2 million people worldwide were
living with dementia in the year 2019, and this number is expected to rise to 78 million in 2030 and
139 million in 2050, with a corresponding increase in the ageing population.
the brain cells, mainly in the hippocampus and cortex, leading to impairment in learning, thinking
-
tau proteins) in the brain.
2,3
neurons (extracellular), tau protein hyperphosphorylation and accumulation occurs inside the
neurons (intracellular). Alzheimer’s disease disrupts the vital processes of neurons, including com-
munication, metabolism and repair, leading to brain shrinkage (brain atrophy). The dysfunction
and loss of cholinergic neurons in the basal forebrain is one of the most prominent components of
the neuropathology of Alzheimer’s disease.
4
The blood- brain disruption, mitochondrial impairment,
associated with AD.
5
The progression of AD is also associated with the depletion of neurotrophins
that regulate the survival, differentiation and function of neurons.
6
Increasing evidence indicates a
7,8
which may be the reason
Although a combination of genetics, lifestyle and environmental factors are implicated, the
greatest risk factor for late- onset Alzheimer’s is old age.
9
The percentage of people with Alzheimer’s
113
Neuroprotective Potential of Traditional Indian Medicinal Plants
of people aged 75 to 84, and 33.2% of people aged 85 or older.
10
The pace at which the symptoms of
dementia advance from mild to moderate to severe also differs from person to person. Cholinesterase
inhibitors increase the availability of acetylcholine at synapses in the brain and are one of the drug
therapies used in the treatment of Alzheimer’s disease dementia. Despite several drugs approved
by the U.S. Food and Drug Administration (FDA), including donepezil, rivastigmine, galantamine,
memantine, and memantine combined with donepezil, there is no cure for Alzheimer’s disease, as
these drugs are unable to halt or reverse the progression of the disease. (www.nia.nih.gov/ hea lth/
how- alz heim ers- dise ase- trea ted)
Parkinson’s disease (PD) is the second most common age- related neurodegenerative disorder,
synuclein in the brain.
11
It is a slow progressive disorder that affects movement, muscle control,
and balance. The motor symptoms of the disease result from the death of cells in the pars compacta
proteins into Lewy bodies within the neurons constitute one of the important pathological hallmarks
of PD.
12
Complex interactions between genetic, environmental and pathological factors, including
13
The clinical symptoms of the disease referred to as Parkinsonism include bradykinesia (slowness of
movement), resting tremors, hypokinesia (decreased amplitude of movement), postural instability
(imbalance and stooped posture), and cogwheel rigidity.
14
The non- motor symptoms of PD include
sleep disturbances, cognitive decline with dementia, orthostatic hypotension and depression.
15
Global estimates in 2019 revealed over 8.5 million individuals with PD (www.who.int/ news- room/
fact- she ets/ det ail/ parkin son- dise ase). The disease is clinically incurable, and disability and death
due to PD are increasing globally.
Levodopa drug, a dopamine precursor, has been widely used for several years in the manage-
ment of Parkinson’s disease, often in combination with carbidopa. Levodopa works by crossing
the blood- brain barrier (BBB), allows neurons to make new dopamine, and reduces the symptoms
of slowness, stiffness and tremors. However, the drug does not stop or slow the progression of the
disease, may cause side effects and may lose effectiveness over time. The adverse effects of the
levodopa drug may include nausea, vomiting, dry mouth, dizziness and confusion, hallucinations,
dyskinesia and psychosis in some patients. (https:// medl inep lus.gov/ drugi nfo/ meds/ a601 068.html).
The immune system plays a complex role in the progression of neurodegenerative disorders and
exhibits both neurodestructive and neuroprotective responses.
6
The brain is prone to oxidative stress,
16
immune response in the brain causes neurodegeneration as well as facilitates and exacerbates
both amyloid and tau core pathologies of Alzheimer’s disease.
17
Microglia and astrocytes, both
types of glial cells, are the key innate immune cells in the CNS. While glia are essential for regu-
lating homeostasis in the normal brain, their dysfunction contributes to neurodegeneration in many
brain diseases, including Alzheimer’s
18
and Parkinson’s disease.
19
Increased microglial activation
and astrocytes have been found in both postmortem AD and PD brains. Over- activated micro-
are common features of Alzheimer’s
20
and Parkinson’s disease.
21
The activated microglial cells are
known to induce an excessive secretion of neurotoxic factors like nitric oxide (NO), reactive oxygen
neuronal damage.
The functional and structural integrity of the BBB is pivotal to maintaining the homeostasis of
the brain microenvironment.
22
The BBB is formed by microvascular endothelial cells lining the