WORLD JOURNAL OF PHARMACY AND PHARMACEUTICAL SCIENCES

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

Volume 3, Issue 5, 234-252. Review Article ISSN 2278 – 4357

AYURVEDIC APPROACH WITH A PROSPECTIVE TO TREAT AND

PREVENT ALZHEIMER’S AND OTHER COGNITIVE DISEASES: A
REVIEW

Kinjal C Patel*, Soma Pramanik, Vibha C Patil

Department of Pharmaceutics and Department of Pharmaceutical Chemistry

Acharya & B M Reddy College of Pharmacy, Soldevanahalli, Hesaraghatta Main Road,
Bangalore- 560107, Karnataka, India.

Article Received on
23 February 2014,
Revised on 24 March
2014,
Accepted on 21 April 2014
*Correspondence for Author
Kinjal C Patel
Department of Pharmaceutics
and Department of
Pharmaceutical Chemistry
Acharya & B M Reddy College
of Pharmacy, Soldevanahalli,
Hesaraghatta Main Road,
Bangalore, Karnataka, India .
treatment of Alzheimer’s disease.
ABSTRACT
Alzheimer’s disease (AD) is the most common form of dementia
which occurs among older people above the age of 60 years.
Alzheimer’s disease is characterized by massive loss of neurons and
disrupted signaling between cells in the brain. The cholinergic deficit
in this disease is responsible for most of the short term memory which
leads to progressive loss of memory, deterioration of all intellectual
functions, increases apathy, decreases speech function, disorientation
and gait irregularities. The currently available drugs for the treatment
of Alzheimer’s disease are having a limited scope, symptomatic only
and produce adverse reactions in the patients. The herbal remedies
become more and more popular in the recent years and also provide
very promising benefits to the patients suffering from AD. The current
paper reviews the clinical effects of a few commonly used herbs for the

Keywords: Alzheimer’s disease, herbal treatment, memory, cognitive disease, dementia.

INTRODUCTION
Rapid changes in life-style, environmental pollution and excessive use of fertilizers and
hazardous toxic chemicals during the production of food materials, are seriously life
threatening for human beings and causing health hazards. These toxic chemicals produce
neurotoxins that affect the transmission of chemical signals between neurons resulting into

www.wjpps.com Vol 3, Issue 5, 2014. 234

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

neurodegenarating disorders. Among different kind of neurodegenarating diseases,

Alzheimer’s disease (AD) is the most common form of the dementia which occurs among the
older people above the age of 60 years[1].

Alzheimer’s disease is a progressive neurodegenerative brain disorder that is slow in onset

but leads to dementia, unusual behavior, personality change and ultimately death[2]. The
prevalence has been found to rise exponentially with age, ranging from 3.0% in patient’s
aged 65-74 years to as much as 47.2% in those aged 85 years[3]. AD is an irreversible,
progressive brain disease that slowly destroys memory and thinking skills and eventually
even the ability to carry out the simplest tasks. World Health organization (WHO) has
estimated that 35.6 million people are currently living with dementia worldwide which will
be further increase to 65.7 million by 2013 and 115.4 million by 2050[4].

The brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others to
form communication networks. Groups of nerve cells have special jobs. Some are involved in
thinking, learning and remembering. Others help us see, hear and smell. Physically,
Alzheimer’s is characterized by massive loss of neurons and disrupted signaling between
cells in the brain. The disease can be diagnosed postmortem by observing tangles inside and
senile plaques outside cells throughout the brain. The major component of the plaque is a
small, 40/42-amino acid peptide amyloid-beta (Aβ). Aβ, causative agent in AD, was first
suggested as the amyloid hypothesis about 15 years ago and is now widely accepted among
scientific community. Aβ is an elusive entity whose chemical and biological action has been
difficult to understand. It is not very soluble, cannot crystallize and has highly changeable
structure in a solution[5].

The studies have indicated that as Alzheimer’s disease progresses, neurofibrillary tangles and
also the plaques spread throughout the brain starting in the neocortex. By the final stage,
damages widespread and brain tissue shrunks significantly. Studies have shown the
involvement of neurotransmitter acetylchloline in Alzheimer’s disease resulting into
disproportionate deficiency of acetylchloline. It has been documented that markers for
cholinergic neurons, acetylcholine transferase and acetylcholine esterase are responsible for
acetylcholine synthesis and its degradation decreases in the cortex and hippocampus area of
the brain involved in cognition and memory[6]. The study has demonstrated that the resultant
decreased in acetylcholine dependant neurotransmission, is associated with the functional
deficit of AD[7].

www.wjpps.com Vol 3, Issue 5, 2014. 235

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

The use of cholinesterase inhibitors in the treatment of patient with Alzheimer disease has
been found to be better successful strategy[8,9]. The tacrine, the acridine derivatives, was the
first drug approved by food and drug administration (FDA), USA for general clinical use in
Alzheimer’s disease. The other four new choline esterase inhibitors approved by FDA, USA
to treat Alzheimer’s are Donepezil (Aricept), Rivastigmine (Exelon), Galantamine
(Reminyl)[10-12].

The above mentioned drugs are used to treat mild to moderately severe Alzheimer’s. The new
drug memantine (nemenda) approved by food and drug administration (FDA), USA in
October 2003, is used for treatment of patient with Alzheimer’s at the moderate to severe
stage of disease. Other drugs such as selegiline, vitamin E, estrogen and anti-inflammatory
drugs have also been studied for treatment of Alzheimer’s, but their clinical use has not been
clearly demonstrated[11,13].

The currently available drugs for the treatment of Alzheimer’s disease do not alter the
condition and progression of the disease. They also produced adverse effects in the patients,
there by cannot use them for prolong time. To alter the current conditions related to present
dosage form, need to search alternative effective therapy, which will alter the present
condition also retard the progression of the disease by preventing the formation or clearing of
plaques.

Herbal medicine treatment for Alzheimer’s disease becomes very popular now a day because
of their activities against AD and slowing down the progression of it. Many herbal medicines
have been researched and the benefits derived from using these medicines for AD and
dementias are promising. Also, these herbs are inexpensive and can be easily available. The
results observed form the treatment with herbal medicines are promising also with fewer
adverse effects. Instead of using synthetic drugs with more side effects, herbals supplements
can be used as their substitutes. In the present review article, we tried our best to present
some of herbal drugs which are using now a day for the treatment of AD. Also, some current
research work going on them to prove their mechanism for slowing down the progression of
AD. Following herbal plants or their parts are used for treatment for AD.

www.wjpps.com Vol 3, Issue 5, 2014. 236

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

Curcuma longa L. (Turmeric, Haridra)

Family: Zingiberaceae
Curcuma Longa L. is an herbal medicine being used in India.
It is cultivated in almost all the state of India. It has
curcuminoids (~6%), the yellow coloring principles, of
which curcumin (diferuloylmethane), constitutes 50-60%[14].
Studies have proved that curcumin has anti-inflammatory and antioxidant activities, and it
also helps in combating Alzheimer’s disease (AD). Regular consumption of this herb helps in
keeping the mind balanced[15].The dose of curcumin can be reduced by making colon
targeting[16]. Crude drug is used in doses of 3-9 g daily[17].

Bacopa monnieri (Linn.) Weltst (Nira Brahmi)

Family: Scrophulariaceae
It has been used in the ayurvedic system of medicine for
centuries. Traditionally, it has been used as a brain tonic to
enhance memory development, learning, and
concentration[18]. Also, it provides relief to patients with
anxiety or epileptic disorders[19]. In ancient Indian
literature, Bacopa has been described as one of most popular medhya drug (Noo-tropic
agent). Several studies have revealed that this medicinal herb is advocated as a nervine and
mental tonic and may be used for the treatment of neurological and mental disorders[20-24].
The constituents which are responsible for Bacopa’s cognitive effects are bacosides A and
B[25]. The triterpenoid saponins and their bacosides are responsible for Bacopa’s ability to
enhance nerve impulse transmission. The bacosides aid in repair of damaged neurons by
enhancing kinase activity, neuronal synthesis, and restoration of synaptic activity, and
ultimately nerve impulse transmission. Loss of cholinergic neuronal activity in the
hippocampus is the primary feature of Alzheimer’s disease. Bacopa has been shown to
decrease whole brain AChE activity which reflects that Bacopa might prove to be an useful
memory restorative agent in the treatment of Alzheimer’s and dementia[26]. A clinical study
on human subjects demonstrated the potential of Bacopa monnieri in the treatment of
neuritis[27]. Dosage of powdered drug is 5-10 g and infusion 8-16 ml[28].

www.wjpps.com Vol 3, Issue 5, 2014. 237

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

Centella asiatica (Mandookparni/ Brahmi)

Family: Apiaceae
It has been demonstrated to possess neuro protective
property[29]. Extract from the leaves of Centella asiatica
has been used as an alternative medicine for memory
improvement in the Indian ayurvedic system of medicine
for a long time[30]. Recent study conducted on transgenic
animal model to evaluate the efficacy of Centella asiatica extract (CaE) in the management
of AD, has shown that CaE can impact the amyloid cascade altering amyloid β pathology in
the brains of PSAPP (presenilin ‘Swedish’ amyloid precursor protein) mice and modulating
components of the oxidative stress response that has been implicated in the
neurodegenerative changes occurring in AD[31].

Ginko biloba (maidenhair tree)

Family : Ginkgoaceae
Ginkgo biloba is a herbal medicine being used in
traditional Chinese medicine for thousands of years to treat
a variety of ailments. It has been shown to reduce memory
loss, enhance the brain activity and to slow down the
degenerative effects of Alzheimer’s disease[32,33]. The broad therapeutic spectrum of Ginkgo
may be explainable in part by the fact that it influences two fundamental aspects of human
physiology: 1) it improves blood flow to the brain and other tissues and 2) it enhances
cellular metabolism. Because these functions are essential for good health, it is not
unreasonable to consider the possibility that Ginkgo might have a broad spectrum of clinical
applications. An extract of Gingko biloba has been found in several studies to improve the
symptoms and slow the progression of Alzheimer’s disease (AD) similar to prescription
drugs such as Donepezil or Tactrin, with minimal undesirable side effects. The ginkolides
present in Ginkgo biloba possess activities pertinent to the disease mechanisms in
Alzheimer’s such as antioxidant, neuroprotective and cholinergic activities according to the
studies conducted by Medical Research Council of New castle General Hospital[34]. Ginkgo
biloba improves protection against Aβ protein-induced oxidative damages (degrading
hydrogen peroxide, preventing lipids from oxidation, and trapping the reactive oxygen
species)[35]. Ginkgo leaf extract contains terpenoids (bilobalides and ginkgolides) and
flavonoid glycosides. Flavones can reduce the fragility of capillaries, and protect the body

www.wjpps.com Vol 3, Issue 5, 2014. 238

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

from blood loss through damaged capillaries, particularly in the brain. The ginkgolides,
particularly ginkgolide B, inhibit the platelet-activating factor and so increase the fluidity of
the blood that improves circulation, again particularly in the micro-capillaries of the brain.
This is also why it is believed to reduce the incidence of cerebral thrombosis and resultant
strokes[36]. Various clinical studies have indicated that 3- to 6-month treatment with 120-
240mg of G. biloba has produced significant effect in Alzheimer’s patients and this herbal
drug has shown no significant adverse effect except few case reports of bleeding
complications, gastrointestinal discomfort, nausea, vomiting, diarrhoea, headache, dizziness,
heart palpitations and restlessness[37-40].

Salvia officinalis (Sage)

Family: Lamiaceae
The extract of Salvia officinalis (sage) has been found to
produce significant benefits in cognition to the patients
with mild to moderate AD after 16 weeks of treatment with
S. officinalis[41]. It contains the antioxidants carnosic acid
and rosmarinic acid. These compounds are thought to
protect the brain from oxidative damage[42].The studies have demonstrated that the side effect
associated with S. officinalis where similar to those observed with cholinesterase
inhibitor[43].However, frequency of agitation appeared to be higher in placebo group which
may indicate an additional advantage in the management of patient with Alzheimer’s disease.

Rosmarinus officinalis (Satapatrika)

Family: Lamiaceae
It contains the following natural COX-2 inhibitors:
Apigenin, carvacrol, eugenol, oleanolic acid, thymol and
ursolic acid. In addition, Rosemary contains antioxidants
and anti-inflammatory compounds. Some of the strongest
antioxidants in the herb are carsonic acid and ferulic acid,
which have even greater reported antioxidant activity than the widely common synthetic
antioxidants Butylated hydroxytoluene (BHT) and Butylated hydroxyanisole (BHA)[44]. The
findings of the study indicate that the olfactory properties of this essential oil can produce
objective effects on cognitive performance, as well as subjective effects on mood[45].It has
been evaluated using different in vitro and in vivo models to prove their efficiency in the

www.wjpps.com Vol 3, Issue 5, 2014. 239

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

management of Alzheimer’s disease patient. The studies have demonstrated that extract from
plants of the lamiaceae family are active not only in the inhibition of AchE or β-amyloid
deposits inhibition in vitro but also may have anti-BuChE (Butyrylcholinesterase) activity. In
addition, the antioxidant, cytoprotective, anti-apoptotic and anti-inflammatory activities have
also been found in lamiaceae plant extracts[46].

Melissa officinalis (Lemon Balm)

Family: Lamiaceae
Melissa officinalis was believed to sharpen memory. Melissa
officinalis has shown to improve cognitive function and to
reduce agitation in patients with mild to moderate AD. Studies
have demonstrated M. officinalis causes ACh receptor activity
in central nervous system with both nicotinic and muscarinic
binding properties[47-48]. This plant has also been reported to modulate mood and cognitive
performance when administered to young and healthy volunteer[49]. So, concluded that M.
officinalis one of several plants that may be useful in the prevention and treatment of
Alzheimer’s disease due to its ability to inhibit acetylcholinesterase and its antioxidant
activity.

Glycyrrhiza glabra (Licorice Root)

Family: Fubaceae
Alzheimer’s disease is characterized by neuronal loss and
the presence of the extracellular senile plaque, whose major
constitute is amyloid-β peptide (Aβ). In that study, it was
investigated the effect of water extract of licorice on Aβ 25-
35- induced apoptosis in PC12 cells. Results suggest that GWE exerts a protective effect
against apoptotic neuronal cell death induced by Aβ fragments. Extract from the licorice root
is reported to treat or even prevent brain cell death in disease like Alzheimer’s and its
associated symptoms[50]. Recent studies have shown that the dose of 150 mg /kg of the
aqueous extract of licorice significantly improved learning and memory of mice[51].

www.wjpps.com Vol 3, Issue 5, 2014. 240

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

Galanthus nivalis (snowdrop) (Alkaloid-Galantamine)

Family: Liliacea
The chief chemical constituent of the Galanthus nivalis is
galantamine, and this is an isoquinoline alkaloid. Clinical
studies on the efficacy of galantamine have demonstrated
its use in the treatment of mild to moderate AD and other
memory impairments. This drug has been found to be a
competitive and selective acetylcholinesterase inhibitor. It is hypothesized that this action
might relieve some of the symptoms of AD. This drug has also been shown to modulate
allosterically nicotine Ach receptors on cholinergic neurons to increase acetylcholine release,
which can be beneficial for the treatment of AD[52].

Huperzia serrata (firmosses)

Family: Licopodiaceae
Huperzia serrata contains a large group of alkaloids called
‘licopodium alkaloids’. Huperzin A, a novel licopodium
alkaloid extracted from Huperzia serrata, is well known as a
reversible, potent and selective AChE inhibitor and
improves memory and mental functioning in patient with alzheimer’s and other severe
conditions[52-54]. This drug has been shown to possess antioxidant and neuroprotective
properties suggesting thereby its potential in the treatment of Alzheimer’s disease[55,56].

Commiphora wighitti (Guggul or Mukul myrrh tree)

Family: Burseraceae
Commiphora wighitti, a plant resin contains a major of
guggulipid, which is guggulusterone Z and E. The
guggulipid has been seen to be a potential cognitive
enhancer for improvement of memory in scopolamine
induced memory deficits[57]. Commiphora wighitti acts on
impairment in learning and memory and decreases choline acetyl transferase levels in
hippocampus. However it shows maximum effect on memory functions and the potential for
dementia disorder[58].

www.wjpps.com Vol 3, Issue 5, 2014. 241

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

Panax ginseng (Ginseng root)

Family: Araliaceae
Panax ginseng contains saponins protopanaxadiol,
protopantriol and oleanolic acid. Saponins that are reported
to have memory enhancing action for the learning
impairment induced by scopolamine[57]. Ginseng has been
shown to exhibit protective and tropic effect in memory
functions of alzheimer’s disease. Clinical study conducted on group of AD patients has
demonstrated that Panax ginseng is clinically effective in the cognitive performance of AD
patients[59]. In addition, the studies conducted to evaluate the efficiency of Panax ginseng in
the treatment of alzheimer’s disease patients have demonstrated significant effect in the favor
of ginseng on the Mini-Mental Status Examination, and on the alzheimer’s disease
assessment scale (ADAS)-cognitive[60]. Research has also suggested that ginseng is able to
enhance the psychomotor and cognitive performance, and can benefit AD by improving the
brain cholinergic function, reducing the level of AD and repairing the damaged neuronal
networks[61].

Tinospora cordifolia (Guduchi)

Family: Menispermaceae
Tinospora cordifolia possesses a memory enhancing
property for learning and memory in normal and memory
deficits animals. Tinospora cordifolia’s mechanism for
cognitive enhancement is by immunostimulation and
synthesis of acetylcholine, this supplementation of choline
enhances the cognitive functions[57].

Withania somnifera (Ashwagandha)

Family: Solanaceae
Withania somnifera has been described as a nervine
tonic[62,63] in ayurveda and that is why it is a common
ingredient of ayurvedic tonics, rejuvenators and vitalizer
appear to ally disease and induced immunity and longivity in
the users[64-66]. The assessment of cholinesterase inhibition
was carried out using a colorimetric method based on Ellman’s reaction and demonstrated

www.wjpps.com Vol 3, Issue 5, 2014. 242

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

that the W. Somnifera extract significantly inhibited AChE in a concentration dependent

manner[67]. Withania somnifera has been shown to slow, stop reverse and remove neuritic
atrophy and synaptic loss, which is the main cause for neurodegenerative disorders including
Alzheimer’s and dementia as confirmed by several clinical studies. Therefore, this herb can
be used for the treatment and management of patient with AD. It improves growth of new
dendrites of neurons. Glycowithanolides withaferin – A and sitoindosides VII-X isolated
from the roots of Withania somnifera have been shown to significantly reverse the ibotenic
acid induced cognitive defects in AD model[68].

Catharanthus roseus (Alkaloid-Vinpocetine)

Family: Apocynaceae
Vinpocetine is a chemical derived from vincamine, a
constituent found in the leaves of Catharanthus roseus, as
well as the seed of various American plants[69].Vinpocetine
is described as a specific inhibitor of basal and calmodulin-
activated phosphodeesterase 1 (PDE1). This effect leads to
an increase of cAMP over cGMP[70]. Vinpocetine has been shown to facilitate long term
potential, enhance the structural dynamics of dendritic spines improve memory retrieval[71],
and enhance performance on cognitive test in humans[72]. Vinpocetine is found to dilate the
cerebral vascular, promote the redistribution of blood flow and favor the aerobic glycolysis
towards damaged areas[73]. Because of this it’s showing neuro protective effects[74]. It is used
as a drug in Eastern Europe for the treatment of cerebrovascular disorders and age related
memory impairment[75]. Several double –blind studies have evaluated vinpocetine for the
treatment of AD and related conditions[76]. It increases level of neuro transmitters like
cholinergic, nor-adrenaline and dopamine associated with spatial working memory tasks[77]
and enhances cognition and memory[78]. Vinpocetine decreases the disrupting effect of
scopolamine on acquisition and prevent the memory loss. It also has been reported that
vinpocetine improves memory and reduce oxidative stress and cholinergic deficit in
experimental model of Alzheimer’s disease[77].

Euphorbia royleana boiss (source of Shilajit)

Family: Euphorbiaceae
Shilajit is a dark, thick, viscous, sticky, unctuous, complex
substance having a number of organic and inorganic

www.wjpps.com Vol 3, Issue 5, 2014. 243

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

compounds flowing out from the rocks occurring in the north western belt of lower
Himalayan hills from Nepal to Kashmir and is known as bitumen or mineral resin[79]. Shilajit
is used in Ayurveda, the traditional Indian system of medicine. It is a rasayan material which
has adaptogenic, antistress and immunomodulatry activities[80]. Studies have demonstrated
the potential of shilajit in the treatment of AD disease[81]. The studies to assess its
effectiveness in the management of AD demonstrate that shilajit affects some events in
cortical and basal forebrain cholinergic signal transduction cascade in rat brain. Studies have
been conducted on drugs that enhance cholinergic activity as potential therapeutic agent in
the treatment of AD. Further, it has also been seen that systemic administration of defined
extracts from the Withania somnifera (Indian ginseng) in combination with shilajit
differentially affects preferentially events in the cortical and basal forebrain cholinergic
signal transduction cascade[82].

Crocus Sativus (Saffron)

Family: Iridaceae
Studies suggest that Crocus Sativus stigmas extract may
have antioxidant and antiamyloidogenic activity, thus
reinforcing ethnopharmacological observation that saffron
has a positive effect on cognitive function[83].The main
carotinoid constituent, trans-crocin-4, the digentibiosyl
ester of crocitin inhibited Aβ fibrillogenosis formed by the oxidation amyloid β-peptide in
AD[84]. Crocin demonstrated cognitive enhancing activity in mice[85].

Eclipta alba (Bhringaraj)

Family: Asteraceae
Eclipta alba leaf extract contains luteolins, which may be
responsible for minimizing cognitive deficit due to
cholinergic disfunctioning. Their profound free radical
scavenging action could insulate neuronal tissues from
degeneration probably by preserving these areas from stress
perturbations. Protection of neuronal tissues may be possibly due to the immune modulatory
actions of Eclipta alba. Therefore, Eclipta alba can serve as a potential memory
modulator[86]. Eclipta alba has been found to activate Na+ K+ ATPase which produces an
elevation in the intracellular concentration of Ca+2. Stimulation of the Ca+2 receptor induces

www.wjpps.com Vol 3, Issue 5, 2014. 244

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

the release of 5-hydroxytriptamine. The enhanced turnover of 5-HT can cause blunting of
aggression and could be of plausible reason for the antiaggressive property of Eclipta alba. In
conclusion, the total aqueous extract of Eclipta alba was found to be efficacious in producing
serenity and masking the constellation of behavioral changes encountered during aggressive
bouts making it a promising naturally derived product[87].

Some others medicinal plants effects in the treatment of Alzheimer’s disease (AD) and are:
Maticaria recutita (Asteraceae), Lipidium meyeii walp (Brassicaceae), Acorus ralamus
(Araceae), Angelica archangelica (Umbelliferae), Colliuronia canadensis (Lamiaceae),
Bentholattia excels (Lecythidaceae), Celastrus peniculatus (Celastraceae), Urtica dioica
(Clusiaceae), etc.

CONCLUSION
The present treatment strategies for the management of patients with Alzheimer’s disease
available in allopathic drugs are approved by Food and Drug Administration (FDA), USA.
These treatment strategies are not satisfactory and not able to cure the disease completely.
Moreover, these drugs are symptomatic and do not alter the current conditions or progression
of the underlined disease. Also they produce various side effects. Therefore, further
exploration can be done for the better treatment with least side effects for Alzheimer’s
disease.

Herbs have a low toxicity compare to allopathic drugs approved by FDA,USA which play a
important role in the early stages of the disease and other conditions involving poor memory
and dementia. The herbal drugs can be used along with the other drugs as supplementary. For
the patients having the history of AD in the family may start taking these supplements to
delay or to reduce the further advancement of the disease. This review is to highlight the
possible role of many herbs which have shown their effectiveness in Alzheimer’s or any other
memory related disorders. The plants mentioned in this article helpful in treating and
managing the disease due to their anti-oxidant, anti-inflammatory, neuroprotective,
procholinergic and anti-acetylcholinesterase properties. Further, large scale studies are
required to determine effectiveness of these herbs in the treatment and management of AD.
Until then, this review will provide some facts regarding the benefit of the herbs mentioned in
the article.

www.wjpps.com Vol 3, Issue 5, 2014. 245

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

REFERENCES
1. Singh N, Pandey BR, Verma P. An overview of phytotherapeutic approach in prevention
and treatment of alzheimer’s syndrome and dementia. Int J PharmaceuSci Drug Res,
2011; 3(3):162-72.
2. Jewart RD, Green J, Lu CJ, Cellar J, Tune LE. Cognitive behavioral and physiological
changes in alzheimer’s disease patient as a function of incontinence medication. Am J
GeriatPsychiat, 2005;13:324-8.
3. Wernicke PF, Reischies FM. Prevelance of dementia in old age; clinical diagnosis in
subjects aged 95 years and older. Neurology,1994; 44: 250-3.
4. Wimo A, Prince M. The Global Economic Impact of Dementia, 2010. Alzheimer’s
disease International, World Alzheimer Report 2010.
5. Rauk A. The chemistry of Alzheimer’s disease. ChemSoc Rev, 2009; 38: 2698-715.
6. Francis PT, Palmer AM, Snape M. The cholinergic hypothesis of Alzheimer's disease: A
review of progress. J NeurolNeurosur Ps, 1999; 54: 137-47.
7. Wright CI, Geula C, Mesulam MM. Neurological cholinesterase in the normal brain and
in Alzheimer's disease: Relation to plaques, tangles, and patterns of selective
vulnerability. Ann Neurol, 1993; 34: 373-84.
8. Nordberg A, Svensson AL. Cholinesterase inhibitors in the treatment of Alzheimer's
disease: A comparison of tolerability and pharmacology. Drug Safety, 1998;19: 465-80.
9. Weinstock M. Selectivity of cholinesterase inhibition: Clinical implication for the
treatment of Alzheimer's disease. CNS Drugs, 1999; 12: 303-7.
10. Bullock R. Drug treatment in dementia. CurrOpinPsychiatr, 2001; 14: 349-53.
11. Bullock R. New drugs for Alzheimer's disease and other dementias. Brit J Psychiat, 2002;
180: 135-9.
12. Keltner NL, Beth Williams SN. Memantine- A new approach to Alzheimer's disease.
PerspectPsychiatr C, 2004; 40: 123-4.
13. Akhondzadeh S, Noroozian M. Alzheimer's disease: Pathophysiology and
pharmacotherapy. I Drugs, 2002; 4: 1167-72.
14. Ohshiro M, Kuroyangi M, Ueno A. Phytochem, 1990; 29: 2201.
15. Available from: http:// www.naturalremediescenter.com. [Last accessed on 2014 Jan 21].
16. Elias EJ, Anil S, Ahmad S, Daud A. Colon targeted curcumin delivery using guar gum.
Nat Prod Commun, 2010; 5: 915-8.

www.wjpps.com Vol 3, Issue 5, 2014. 246

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

17. The pharmacopoeia of the people’s Republic of China (English Edition); Guangdong
Science and Technology Press, Guangzhou, China 1992;156.
18. Mukheijee DG, Dey CD. Clinical trial on Brahmi. J Exper Med Sci, 1966; 10: 5-11.
19. Chopra RN. Indigenous Drugs of India. 2nd ed., Calcutta; India: U.N. Dhar and
Sons:1958, pp. 41.
20. Abbas SS, Singh V, Bhalla M, Singh N. Clinical Study of Organic Aswagandha in cases
of Parkinsonism, Neuropathy, Paralysis and Uterine Tumors ( Fibroids and Other
Tumours) including Cutanious endodermal carcinoma, National Seminar on Eco-friendly
Herbs of Ayurveda in the Health-care of Mankind: A strategy for Scientific Evaluation
and Uniform Standardization. 2004, pp. 15-16.
21. Chopra RN, Chopra IC, Handa KN, Kapur LD. Indigenous Drugs of India. 2nd ed.,
Calcutta; UN Dhar and Sons Pvt. Ltd.: 1958.
22. Satyavati AY, Raina MK, Sharma M. Medicinal plants of India. Vol I, New Delhi; Indian
council of Medical Research: 1976.
23. Khory RN, Katrak NN. MateriaMedica and Their Therapeutics. Delhi; Neeraj Publishing
House: 1981.
24. Asolkar LV, Kakkar KK, ChakreOJ. Second supplement to glossary of Indian Medicinal
plants with Active Principles.Part 1 (A-K) (1965-1981), New Delhi; PLD (Council of
Scientific and Industrial Research): 1992.
25. Kapoor LD. CRC Handbook of Ayurvedic Medicinal Plants. Boca Raton, FL; CRC Press
Inc: 1990, pp. 61.
26. Joshi H, Parle M. Brahmirasayana improves learning and memory in mice. Evid Based
Complement Alternat Med, 2006; 3(1): 79-85.
27. Bhalla M, Raghuvanshi P, Sharma SC, Singh N. Management of Neuritis and
Parkinsonism by Bacopamonnieri. In the Proceedings- Relevance of Modern Methods of
Pharmacological Studies to Traditional Medicine, 2008, pp. 77.
28. Kapoor LD., Hand book of Ayurvedic medicinal plants.61, Florida; CRC Press: 1990.
29. Lee MK, Kim SR, Sung SH, Lim D, Kim H, Choi H et al. Asiatic acid derivatives protect
cultured cortical neurons from glutamate-induced excitotoxicity. Res
CommunMolPatholPharmacol, 2000; 108: 75–86.
30. Singhal AK, Naithani V, Bangar OP. Medicinal plants with a potential to treat Alzheimer
and associated symptoms. IntJ NutrPharmacolNeurol Dis, 2012; 2(2): 84-91.

www.wjpps.com Vol 3, Issue 5, 2014. 247

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

31. Dhanasekaran M, Holcomb LA, Hitt AR, Tharakan B, Porter JW, Young KA et al.
Centellaasiatica Extract Selectively Decreases, Amyloid β Levels in Hippocampus of
Alzheimer’s disease Animal Model. Phytother Res, 2009; 23: 14-9.
32. DeKosky ST, Williamson JD, Fitzpatrick AL,Kronmal RA, Lves DG, Saxton JA et
al.Ginkgo biloba for prevention of dementia: a randomized controlled trial. JAmMed
Assoc, 2008; 300(19): 2253-62.
33. Alan RG.Ginkgo biloba Extract: A Review. Alter Med Rev. 1996; 1(4): 171-9.
34. Perry EK, Pickering AT, Wang WW, Houghton PJ, Perry NS. Medicinal plants and
Alzheimer's disease: from ethnobotany to phytotherapy. Medical Research Council,
Newcastle General Hospital, Newcastle upon Tyne. J Pharm Pharmacol, 1999; 51(5):
527-34.
35. Available from :http://www.richeters.com.[Last accessed on 2014 Feb 21]
36. Sandrine A, Sophie G, Karine A, Fati N, Emma R. Alzheimer’s disease onset with
Ginkgo biloba and other symptomatic cognitive treatments in a population of women
aged 75 years and older from the EPIDOS study. J Gerontol ABiolSciMedSci, 2003; 58:
372-7.
37. Kanowski S, Hoerr R. Proof of the efficacy of the Ginkgo biloba special extract egb761
in outpatients suffering from mild to moderate primary degenerative dementia of the
Alzheimer type of multi-infarct dementia. Phytomedicine, 1997; 4: 215-22.
38. Le Bars PL, Katz MM, Berman N, Itil TM, Freedman AM, Schatzberg AF. A placebo-
controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia.
North American EGb Study Group. J Am Med Assoc 1997; 278: 1327-32.
39. DeFeudis FG. In: DeFeudis FV(ed). Ginkgo bilobaExtract (EGb 761): Pharmacological
Activities and Clinical Applications, Paris; Scientifiques Elsevier: 1991, pp. 7-146.
40. Kleijnen J. Ginkgo biloba. Lancet, 1992; 340: 1136-9.
41. Akhondzadeh S, Noroozian M, Mohammadi M, Ohadinia S, Jamshidi AH, Khani M.
Salvia officinalis extract in the treatment of patients with mild to moderate Alzheimer's
disease: A double blind, randomized and placebo-controlled trial. J Clin Pharm Ther,
2003; 28: 53-9.
42. Duke JA. Rosemary, the herb of rememberance for Alzheimer’s Disease. Altern
Complement Ther, 2007; 287-90.
Available from: http://www.suite101.com

www.wjpps.com Vol 3, Issue 5, 2014. 248

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

43. Wake G, Court J, Pickering A, Lewis R, Wilkins R, Perry E. CNS acetylcholine receptor
activity in European medicinal plants traditionally used to improve failing memory. J
Ethnopharmacol, 2000; 69: 105-14.
44. Available from :http://www.associatedcontent.com
45. Moss M, Cook J, Wesnes K, Duckett P. Aromas of rosemary and lavender essential oils
differentially affect cognition and mood in healthy adults. Int J Neurosci, 2003; 113(1):
15-38.
46. Ożarowski M, Mikołajczak P Ł, Bobkiewlcz-Kozłowska T, Kujawski R, Mrozikiewicz P
M. Neuroactive compounds from medicinal plants of the Lamiaceae family showing
potentially beneficial activity in treatment of Alzheimer's disease. Herba Pol, 2009; 55(4):
148-63..
47. Perry EK, Pickering AT, Wang WW, Houghton PJ, Perry NS. Medicinal plants and
Alzheimer's disease: from ethnobotany to phytotherapy. Medical Research Council,
Newcastle General Hospital, Newcastle upon Tyne. J Pharm Pharmacol,1999; 51(5): 527-
34.
48. Perry EK, Pickering AT, Wang WW, Houghton P, Perry NS. Medicinal plants and
Alzheimer's disease: Integrating ethnobotanical and contemporary scientific evidence. J
AlternComplement Med, 1998; 4(4): 419-28.
49. Kennedy DO, Scholey AB, Tildesley NT, Perry EK, Wesnes KA. Modulation of mood
and cognitive performance following acute administration of Melissa officinalis (lemon
balm). PharmacolBiochem Be, 2002; 72: 953-64.
50. Bilge S, Ilkay O. Discovery of drug candidates from some. Turkish plants and
conservation of biodiversity. Pure ApplChem, 2005; 77: 53-64.
51. Dhingra D, Parle M, Kulkarni SK. Memory enhancing activity of Glycyrrhizaglabra in
mice. J Ethnopharmacol, 2004; 91(2-3): 361-5.
52. Ashani Y, Peggins JO III, Doctor BP. Mechanism of inhibition of cholinesterases by
huperzine A. BiochemBiophRes Co, 1992; 184: 719–26.
53. Raves ML, Harel M, Pang YP, Silman I, Kozikowski AP, Sussman JL. Structure of
acetylcholinesterasecomplexed with the nootropic alkaloid. huperzine A. Nat StructBiol,
1997; 4: 57-63.
54. Pang YP, Kozikowski AP. Prediction of the binding sites of huperzine A in
acetylcholinesterase by docking studies. J Comput Aided Mol Des, 1994; 8: 669–81.

www.wjpps.com Vol 3, Issue 5, 2014. 249

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

55. Kozikowski, Alan P, Tueckmantel, Werner. Chemistry, pharmacology, and clinical

efficacy of the chinesenootropic agent huperzine A. Accounts Chem Res, 1999; 32(8):
641–50.
56. Zhang RW, Tang XC, Han YY, Sang GW, Zhang YD, Ma YX et al. Drug evaluation of
huperzine A in the treatment of senile memory disorders. Zhongguo Yao Li XueBao,
1991; 12: 250–2.
57. Lannert H, Hoyer S. Intracerebroventricular administration of streptozotosin causes long
term diminutions in learning and memory abilities and in cerebral energy metabolism in
adult rats. BehavNeurosci, 1998; 112: 1199-208.
58. Rubio J, Qiong W, Liu X, Jiang Z, Dang H, Chen SL, et al., Aqueous extract of black
maca (Lepidiummeyenii) on memory impairment induced by ovariectomy in mice.
EvidBased Complement AlternatMed, 2011, 7 pages. Available from:
http://www.hindwai.com/journals/ecam/2011/253958
59. Lee ST, Chu K, Sim JY, Heo JH, Kim M. Panax ginseng enhances cognitive performance
in Alzheimer disease. Alzheimer Dis AssocDisord, 2008; 22(3): 222-6.
60. Gotez J, Schonrock N, Vissel B, Ittner L. Alzheimer's disease selective vulnerability and
modeling in transgenic mice. J AlzheimerDis, 2009; 18: 243-51.
61. Ahn JY, Kim S, Sung EJ, Ha TY. Effect of licorice (Glycyrrhizauralensisfisch) on
amyloid-β-induced neurotoxicity in PC12 cells. Food SciBiotechnol, 2010;19(5): 1392-5.
62. Singh N. Effect of Withania somnifera and Panax ginseng on dopaminergic receptors in
rat brain during stress. XXXVIth Annual Congress on Medicinal Plant Research
(Freiburg), 28. 1988.
63. Singh N, Misra N. Experimental methods tools for assessment of anti-stress activity in
medicinal plants. J Biomed Res, 1993; 12(182): 124-7.
64. Singh N, Singh SP, Nath R, Singh DR, Gupta ML, Kohli RP et al. Prevention or
Urethane-induced lung adenomas by Withaniasomnifera (L.) Dunal in albino mice. Int J
Crude Drug Res, 1986; 24(2): 99-100.
65. Abbas SS, Singh V, Bhalla M, Singh N. Clinical Study of Organic Aswagandha in cases
of Parkinsonism, Neuropathy, Paralysis and Uterine Tumors ( Fibroids and Other
Tumours) including Cutanious endodermal carcinoma, National Seminar on Eco-friendly
Herbs of Ayurveda in the Health-care of Mankind: A strategy for Scientific Evaluation
and Uniform Standardization, 2004: 15-6.
66. Singh N, Gilca M. Herbal Medicine – Science embraces tradition – a new insight into the
ancient Ayurveda. Lambert Academic Publishing: 2010, pp.520.

www.wjpps.com Vol 3, Issue 5, 2014. 250

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

67. Sadhu JS, Shah B, Shenoy S, Chauhan S, Lavehar GS, Padhi MM. Effects of
Withaniasomnifera ( Ashwagandha) andTerminaliaarjuna (Arjuna) on physical
performance and cardiorespiratory endurance in healthy young adults. Int J Ayurveda
Res, 2010; 1: 144-9.
68. Bhattacharya SK, Goel RK, Kaur R, Ghosal S. Anti - stress activity of Sitoindosides VII
and VIII. New Acylsterylglucosides from Withaniasomnifera. Phytother, 1987; 1: 32-7.
69. Lorincz C, Szász K, Kisfaludy L. The synthesis of ethyl apovincaminate.
Arzneimittelforschung, 1976; 26 (10a): 1907.
70. Denoble VJ. Vinpocetine enhances retrieval of a step-through passive avoidance response
in rats. PharmacolBiochemBehav, 1987; 26: 183-6.
71. Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant
patients suffering from mild to moderate organic psychosyndromes, IntClinPsychopharm,
1991; 6(1): 31–43.
72. Rischke R, Krieglstein J. Protective effect of vinpocetine against brain damage caused by
ischaemia. Jpn J Pharmacol, 1991; 56(3): 349-56.
73. Groo D, Palosi E, Szporny L, Effects of vinpocetine in scopolamine-induced learning and
memory impairments. Drug Develop Res, 2004; 11: 29- 36.
74. Dézsi L, Kis-Varga I, Nagy J, Komlódi Z, Kárpáti E. Neuroprotective effects of
vinpocetine in vivo and in vitro. Apovincaminic acid derivatives as potential therapeutic
tools in ischemic stroke. Acta Pharm Hung, 2002; 72 (2): 84 -91.
75. Monograph: Vinpocetine. Alternative Medicine Review. 2002; 7 (3): 240–3.
76. Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia.
Cochrane Database Syst Rev. 2003; (1):CD003119.
77. Deshmukh R, Sharma V, Mehan S, Sharma N, Bedi KL. Amelioration of
intracerebrovetricularstreptozotocin induced cognitive disfunction and oxidative stress by
vinpocetine- A Pde one inhibitor. Eur J Pharmcol, 2009; 620: 49-66.
78. Hindmarch I, Fuchs HH, Erzigkeit H. efficiency and tolerance of vinpocetine in ambulant
patients suffering from mild to moderate organic psychosyndromes. IntClin Psycho
Pharmacol. 1991; 6(1): 31-43.
79. Hooker JD. Flora of British India. Vol. V,Delhi; BSMPS Dehradun and periodicals
Experts: 1973.
80. Winston D, Maimes S. Adaptogens. Herbs for Strength, Stamina, and Stress Relief,
Healing. Arts Press: 2007.

www.wjpps.com Vol 3, Issue 5, 2014. 251

Kinjal et al. World Journal of Pharmacy and Pharmaceutical Sciences

81. Mukherjee B. Traditional Medicine. In the Proceedings of an International Seminar. 7-

9,New Delhi; Oxford & IBH Publishing: 1992, pp. 308-19.
82. Schliebs R, Liebmann A, Bhattacharya SK, Kumar A, Ghosal S, Bigl V. Systemic
administration of defined extracts from Withania somnifera (Indian Ginseng) and Shilajit
differentially affects cholinergic but not glutamatergic and GABAergic markers in rat
brain. NeurochemInt, 1997; 30(2): 181-90.
83. Schmidt M, Betti G, Hensel A. Saffron in phytotherapy: pharmacology and clinical uses.
Wien Med Wochenschr, 2007; 157: 315-9.
84. Zarghani NS, Heinz D. Monoterpene aldehydes and isoforone related compounds of
saffron. Phytochemistry,1971; 10(11): 2755-61.
85. Abe K, Saito H. Effect of saffron extract and its constituent crocin on learning behavior
and long term potentiation. PhytotherRes, 2000; 14: 149-52.
86. Banji O, David B, Annamalai A, Rand M. investigation on the effect of Eclipta alba on
animal models of learning and memory. Indian J PhysiolPharmacol, 2007; 51(3): 247-51.
87. Otilia JL, David B. Evaluation of antiaggressive activity of Eclipta alba in experimental
animals. Pak J Pharm Sci, 2008; 21(2): 195-9.

www.wjpps.com Vol 3, Issue 5, 2014. 252