Convolvulus pleuricaulis is used in traditional systems of medicine in the treatment of anxiety, neurosis, insanity, and epilepsy, and also as a brain tonic. The whole plant is one of the most important medhya rasayana drugs in Ayurveda. It improves balance and vitiation in kapha-vata-pitta doshas (physiological functions), and the herb is astringent and bitter. C. pleuricaulis is used traditionally to treat nervous debility, insomnia, fatigue, low energy levels, and as a brain tonic, alterative, and febrifuge. The whole herb is used medicinally in the form of a decoction along with cumin and milk in fever, nervous debility, and memory loss. The plant is reported to be a prominent memory improving drug, psychostimulant, and tranquilizer, and it reduces mental tension. The methanolic extract of C. microphyllus Sieb. Ex Spreng (C. pleuricaulis Choisy) showed enhanced release of nerve growth factor (NGF). NGF prevents experimentally induced or age related degeneration of basal fore-brain cholinergic cell bodies in adult rats and can also restore lesion-induced loss of cognitive functions [49, 50].
Also called a kunkumam or keshara in Ayurveda. It is a small perennial cultivated in certain parts of the Jammu, Kashmir, Himachal Pradesh, and Uttarakhand states of India. The medicinally useful part is the stigma, which is dried and marketed as saffron. The important constituents of saffron are its pigments (crocin-1,2,3,4) and essential oils. Four crocetins (F, G, H, I) have also been isolated . The alcoholic extract of saffron ameliorates the impairment effect on learning and memory processes. It has been also shown that crocin inhibits neuronal death induced by both internal and external apoptotic stimuli , thus it is considered as neuroprotector. Crocin prevents the activation of c-jun kinase phosphorylation, which is involved in the signaling cascade for neuronal death .
Curculigo is locally called kalimusli and is found all over India. Pharmacological investigations revealed that the 70% ethanol extract of the rhizomes are a sedative and anticonvulsant. The plant is known to contain steroids and triterpenoids and several phenolic compounds [54, 55].
Curcuma longa is a perennial rhizomatous plant growing all over India. Curcumin or C. longa extract shows strong antioxidant activity. ß-amyloid-induced oxida-tive stress appears to be an important pathway of neuronal cell death in AD. The methanolic extract of turmeric led to the isolation of Calebin-A and the curcum-ins, which effectively protects neuronal cells against ß-amyloid deposition. In another study, curcumin, on oral administration to alcohol-fed rats, caused a significant reversal of brain lipid peroxidation, thus indicating a neuroprotective role . In vivo experiments showed that oral intake of curcumin significantly reduces the duration and clinical severity of demylenation in experimental allergic encephalitis .
Known as mustaka in Ayurveda, Cyprus rotundus is a perennial grass growing almost everywhere in India. Its tubers contain medicinally useful essential oils (sesquiterpenoids, monoterpenes, aliphatic alcohols, acetates). A receptor binding assay demonstrated that isocurcuminol, a constituent of C. rotundus, modulates GABAergic neurotransmission via enhancement of endogenous receptor ligand binding, and thus having a bearing in epilepsy .
In Ayurveda, it is claimed that the leaves of Ficus religiosa possesses anticonvulsant activity. The leaf extract was evaluated for its activity against pentylenetetrazole (PTZ, 60mg/kg i.p.) induced convulsions in albino rats. The study revealed 80 to 100% protection against PTZ induced convulsions when given 30 to 60 min prior to the induced convulsions .
An extract prepared from green leaves (EGB761) was identified as therapeutically useful for the treatment of peripheral circulatory disturbances, as it is a vasodilator. Results showed that EGB761 is not a vasodilator in the classical sense, but it is a CNS function modulating and neuroprotective agent, sustainable for the therapy of patients with cerebrovascular disorders or cerebral insufficiencies. Ginkgo is widely used in Europe for treating dementia. It improves blood flow in the brain and contains flavonoids that act as antioxidants. It is presumed that ginkgo may improve thinking, learning, and memory, and results are very encouraging in people with AD .
More than 40 components of ginkgo have been identified and isolated. Two of the most important groups of active chemicals are flavonoids (quercetin, kaempferol, isorhemnetin) and terpenes (lactones or terpenoids, which include bilobalide and several ginkgolides A, B, C, J and M). Individual constituents have been studied in hundreds of in vitro, animal and human experimental systems [61, 62]. Recently, efforts have been made to understand the effects of ginkgo on dementia of the Alzheimer's type and in the closely related multi-infarct dementia. These doubleblind randomized trials in patients have shown that EGB761 is efficacious in delaying the clinical deterioration with dementia, or in bringing about symptomatic improvement [63-65]. The mechanism of ginkgo's therapeutic effects are not fully understood, but they are attributed to the synergistic effects of its constituents [66, 67]. These act to varying degrees as scavengers of free radicals and chemicals, implicated in the pathophysiology of AD. The dose is 40 mg, three times a day, of an extract standardized to 24% flavonoid, glycoside, and 6% terpenoid.
In Ayurveda Mucuna pruriens is called atmagupta or kapikacchu. It is a herbaceous creeper growing in several parts of India. Its seeds, roots and pod bristles are medicinally useful parts. An important chemical constituent of the plant is the nonprotein amino acid L-dopa, which is present in seeds. In addition, p-sitosterol, lecithin, glutathione, and gallic acid are other important constituents [45, 68-70]. Beans of this plant are used as nutritive food in some parts of India. It is also used as a therapeutic agent in various reproductive and nervous diseases [71-73]. An Ayurvedic formulation containing M. pruriens beans is used in the treatment of Parkinson's disease.
The plant of Nardostachys jatamanasi is used by Santhal tribals in the treatment of madness, epilepsy, loss of unconsciousness, convulsions, etc., . The decoction of the root is also reported to be useful in mental disorders, insomnia, etc. N. jatamanasi is reported to yield 2% volatile oil containing an ester, an alcohol and two alkaloids [75,76]. The rhizome of jatamanasi yields jatamanashic acid [77, 78]. Various extracts of jatamanasi root showed sedative effects in rats. The ethanolic extract of N. jatamanasi reduced rat brain serotonin, and though it showed no effect on the CNS, but oil from the rhizome showed depressant action on the CNS . A preparation comprising N. jatamanasi, Centella asiatica, Acorus calamus, Rau-wolfia serpentina, Saussurea lappa, and Valeriana wallichii showed significant improvement in case of schizophrenic patients . The ethanol extract showed potent inhibition of acetylcholinesterase reaction rate .
This plant is called chitraka in Ayurveda. It is a perennial shrub growing wild in the hotter parts of India. Its roots and root bark are medicinally useful. The chief constituent is plumbagin. The ehanol extract of the root has shown spontaneous motility in rats with a concomitant increase in dopamine and a metabolite ho-movanillic acid level in striatum, indicating a dopaminergic pathway for stimulatory action on the CNS . The plant has also been useful in the treatment of schizophrenia.
In Ayurveda Semecarpus anacardium is commonly known as bhallataka. The tree commonly grows in the hotter areas of India and the foothills of the Himalayas. The fully developed nut is valued medicinally. A phenolic glycoside, anacardoside, has been isolated. Besides the phenol, several biflavonoids have been obtained from the defatted nuts of the plant. A cytological and ultrastructural study on Swiss rats from the author's laboratory has shown neuroprotective effects of the ethanol extract [82-84].
The Swertia chirayita is known as kiraatatikta in Ayurveda and chiraytta is its Indian trade name. It grows in the temperate Himalayas from Kashmir to Bhutan. Though the root is considered more potent, the whole herb is used medicinally. More than 20 n-polyhydroxylated xanthones, such as swertianin, swerchirin, and mangiferin, identified. Mangiferin has been shown to be free radical scavenger  and a superoxide scavenger. It is an inhibitor of the expression of inducible nitric oxide synthatase and TNF genes, thus revealing its potential for the treatment of neurodegenerative disorders .
Withania somnifera is commonly known as ashwagandha in Ayurveda. It is an evergreen shrub growing throughout the drier and subtropical parts of India. The medicinally valuable part is its root, which is used in Ayurvedic preparations. It is used as a powder, decoction, medicated wine, etc. The main pharmacologically active constituents are alkaloids (withanine, cuscohygrine, tropane, anahygrine, somniferin, anaferine, withananine, withananinine) and steroid lactones (withanolides). The total alkaloid content of its roots varies between 0.1 and 0.3%, although in some cases a higher yield is also been reported. Karnic  suggested that W. somnifera should be considered the premier herb for all negative conditions associated with ageing. Evidences shows that the drug is useful in preventing senile dementia and AD . The drug helps in slowing down the progression of AD . Glycowithanolides were also found to reverse both cognitive deficits and perturbed central cholinergic markers induced as a result of neurodegeneration. Bhattacharya et al. , while studying foot shock induced changes in the rat brain, showed that W. somnifera also normalized SOD and LPO activity and enhanced CAT and GPX activity. Its inclusion as a rasayana drug is supported by several studies showing the neuropro-tective activity of W. somnifera roots. Damage to neuron circuits in the brain leads to several diseases, such as memory deficit, AD, and Parkinson's disease. In vitro investigation using the methanolic extract of its roots demonstrated the formation of dendrites. This resulted in a significant increase in the percentage of cells with neuritis in human neuroblastoma SK-N-SH cells . A study in our laboratory showed that the root extract significantly protected the neurons in the hippocampal regions of rats under stress conditions . Oral administration of the root extract improved memory acquisition and retention in experimental animals . The effects of the methanolic extract on cholinergic, GABAergic, and glutamatergic receptors have also been demonstrated in wistar rats, as well as activation of cholinergic signal transduction cascade in the cortical and basal forebrain region .
14.6 Plants not Native to India 14.6.1 Galanthus wornorii
Galanthamine is a pure unaltered extract of Galanthus wornorii . A recent study by Willcock and coworkers  has shown that galanthamine appears to slow the progression of neurodegenerative conditions. It also reversibly and competitively inhibits acetylcholinesterase and enhances the response of nicotinic receptors to acetylcholine. A study in 653 Alzheimer's patients showed that galanthamine slows down the decline of the functional abilities as well as cognition.
Huperzine A was identified for the first time in a Chinese medicinal herb, H. serrata. In a well designed placebo-controlled trial using huperzine, 58% of the patients with AD showed significant improvement in memory and cognitive and behavioral functions after taking 200 mg of the drug, twice per day, for up to 8 weeks. Another double-blind experiment using injected huperzine A also confirmed positive effects in patients with dementia .
Another type of neurodegenerative disease is epilepsy. Lavandula has been used for a long time in traditional medicine as anticonvulsant. Gilani et al.  validated its anticonvulsant effects. The study revealed that an aqueous methanolic extract (600 mg/kg) significantly reduced the severity and increased the latency of onset of convulsions induced by PTZ. Moreover, in isolated rabbit jejunum preparations, it caused a dose dependent relaxation of spontaneous contraction and inhibited K+induced contractions, suggesting Ca+ channel blockade .
The use of medicinal plant products in the form of household formulations, or traditional Indian medicinal systems has been in practice for a long time. Efforts made during the past few decades by systematic experimental and clinical studies have confirmed that several of these products are indeed therapeutically potent, not only in treating cough and cold, but also diseases of the CNS, including neurodegener-ative diseases, for which only symptomatic treatment is available so far. Although all active principles and their mode of action are not yet precisely defined, available data on their neurophamacological activity indicate that they could be sources of better therapy for diseases for which treatment is not yet fully developed. Extracts prepared from many medicinal plants contain a variety of bioactive molecules. Unfortunately, it is extremely difficult to analyze them because of their complex syner-gistic activity.
Acknowledgements The author is grateful to Dr. S.D. Shukla and Mr. D. Sharma (TRF) for their help in prearing this manuscript.
1. Seth PK, Kakkar P (2002) Annl Neurosci 9:17
2. Bhatnagar M (2005) Mol Cellular Neuobiology. Narosa, New Delhi
3. Rajini M, Kanaki NS (2008) Phytochemical standardization of herbal drugs and polyherbal formulations. In: Ramawat KG, Merillon JM (eds) Biotechnology: Bioactive Molecules. Springer, Berlin Heidelberg New York, p 349
4. Puri HS (1970) Q J Crude Drug Res 10:1555
5. Puri HS (1970b) Indian Drugs7:15
7. Puri HS (1972) Indian Drugs 9:11
9. Puri HS (2003) Ayurvedic Herbs of Rejuvenation and Longevity. Taylor and Francis, London
10. Walton J (1998) Oxford University Press, Oxford
11. Gonzalo-Ruiz A, San ZJM, Geula C, Gonzalo P (2005) J Chem Neuroanat 29:31
12. Houghton PJ, Howes M-J (2005) Neurosignals 14:6
13. Maxwell SRJ (1995) Drugs 49:345
14. Jain S, Shukla SD, Sharma K, Bhatnagar M (1998) Indian J Gerontol 12:60
15. Bast A, Haenen GR, Dolemea GJ (1991) Am J Medical 91:2
16. Ghosal S (1991) Indian J Indigen Med 8:1
17. Bhattacharya SK, Kumar A, Ghosal S (1995) Phytother Res 9:110
18. Shukla SD (2001) Ph D thesis, MLS University, Udaipur, India
19. Panda S, Kar A (1997) Ind J Physiol Pharmacol 41:424
20. Cragg GM, Newman DJ, Sanders KM (1997) J Nat Prod 60:52
21. Satyavati GV, Raina MK, Sharma M (1976) Medicinal Plants of India. ICMR, New Delhi
22. Dhawan BN, Shrimali RC (1995) Indian J Pharmacol 27:202
23. Singh HK, Dhawan BN (1997) Indian J Pharmacol 29:5359
24. Shukla PK, Khanna VK, Ali MM, Mayura RR, Handa SS, Srimal RC (2002) Phytother Res 16:256
25. Rastogi RP, Mehrotra BN (1998) Comp Ind Med Plants 5:107
26. Parihar MS, Hemnani T (2004) J Neural Transmiss 111:1
27. Tripathi YB, Chaurasia S, Tripathi E, Upadhyaya A, Dubey GP (1996) Indian J Exp Biol 34:521
28. Saxena, G, Singh M, Saxena A, Bhatnagar M (2007) J Herb Med Toxicol 2:33
29. Saxena G (2005) Ph D thesis, MLS University, Udaipur, India
30. Dhawan BN, Singh H (2002) Ann Neurosci 9:34
31. Rastogi RP, Dhar ML (1960) J Sci Ind Res 19b:455
32. Chatterji N, Rastogi RP, Dhar ML (1963) Indian J Chem 1:212
33. Chatterji N, Rastogi RP, Dhar ML (1965) Indian J Chem 3:24
34. Kawai K, Istaka Y, Shibata S, Kulshreshtha DK, Ratogi RP (1973) Acta Cryst 29B:2497
35. Rastogi S, Pal R, Kulshrestha DK (1993) J Heterocycl Chem 2:149
36. Rastogi S, Kulshrestha DK (1999) Indian J Chem 38b:353
37. Garai S, Mahto SB, Ohtani K, Yamasaki K (1996) Phytochemistry 42:815
38. Bhattacharya SK, Kumar A, Ghosal S (1999) Pharmacol Toxicol 4:11
39. Kumar MH, Gupta YK (2002) Phytomedicine 9:302
40. Joglekar GC, Balwani JM (1967) J Res Indian Med 1:190
41. Lewis WH, Elvin-Lewis MPF (2003) Medical Botany. Wiley, New York p 527
42. Kakrani HK, Nair GV, Kalyani GA, Satyanarayan D (1985) Fitoterapia 56:293
43. Karranth KS, Haridas KK, Gunasundarai S, Guruswami MN (1980) Arogya Health Sci VI:137
44. Nalini K, Aroor AR, Kumar KB, Rao A (1986) Alt Med 1:355
45. Dev S (2006) Prime Ayurvedic Drugs. Anamaya, New Delhi, p 105
46. Kumar MHV, Gupta YK (2002) J Ethanopharmacology 79:253
47. Lee MK, Kim SR, Sung SH, Lim D, Kim H, Choi H, Park HK, Te S, Ki YC (2000) Res Commun Mol Pathol Pharmacol 108:75
48. Khare CP (2006) Indian Medicinal Plants. Springer, Berlin Heidelberg New York, p 169
49. Pavia MR, Davis RE, Schwartz RO (1990) Ann Rep Med Chem 25:21
50. Singh RH, Mehta J (1977) Indian Med Yoga Homeopathy, 12:18
51. Li YC, Wu TS (2001) Chem Pharm Bull 50:1305
52. Soeda S, Iwata K, Hosoda Y, Shimeno H (2001) Life Sci 69:2887
53. Ochiai T, Soeda S, Ochno S, Tnka H, Shoyama Y, Shimeno H (2004) Neurochem Int 44:321
54. Tandon M, Shukla YN (1995) Curr Res Med Aromat Plants 17:42
55. Valls J, Rchard T Larronde F, Leblais V, Muller B, Delauney, JP, Ramawat KG, Merillon JM (2006) Fitoterapia 77:416
56. Aggarwal BB, Shishodia S, Young-Joon S (2007) The Molecular Targets and Therapeutic Uses of Curcumin in Health And Disease. Springer, Berlin Heidelberg New York
57. Natrajan C, Bright JJ (2002) J Immunol 168:6506
58. Ha JH, Lee KY, Choi HC, Cho J, Kong BS, Lim JC, Lee DU (2002) Biol Pharm Bull 25:128
59. Indurwale NH, Biyani KR (2001) Adv Pharmacol Toxicol 2:51
60. Watnabe CMH, Wolffram S, Ader P, Rimbach G, Pecker L, Maguire JJ, Schultz PG, Gohil KC (2001) Proc Natl Acad Sci USA 98:6577
61. Chavez ML, Chavez PI (1998) Hosp Pharm 33:658
62. Van Beek TA, Bombardelli E, Morazzoni P, Peterlongo F (1998) Fitoterapia 69:195
63. Le Bars PL, Katz MM, Berman N, Itil TM,Fredman AM, Saltzberg AFA (1997) JAMA 278:1327
64. Oken BS, Storzbach DM, Kaye JA (1998) Arch Neurol 55:1409
65. Sivarajan VV, Balchandran I (1999) Ayurvedic Drugs and Plant Sources. Oxford & IBH, New Delhi
66. Behl C, Davis J, Leslie R, Schubert D (1994) Cell 77:817
67. Maitra I, Marcocci L, Droys-Lefais M, Packer L (1995) Biochem Pharmacol 49:1649
68. Manyam BV, Parikh KM (2002) Ann Neurosci 9:40
69. Vaidya ND (1925) A Treatise on Experianced Remedies. Vaidya Kalpatru, Ahemdabad, p 100
70. Vaidya AB, Rajgopalan TG, Mankodi NA, Antarkar DS, Tatehd PS, Purohit AV, Wadia NH (1978) Neurol India 26:171
71. Maw GN (1999) Annu Rep Med Chem 34:74
72. Dutt VC (1980) Materia Medica of Hindus (Krishnades Sanskrit Studies, vol II) Varanasi 148-149
73. Damodaran M, Ramaswami R (1937) Biochem 31:2149
75. Jain SK, Tarafdar CR (1970) Econ Bot 24:241
76. Bose BC, Vijayavergia R, Bhatnagar JN (1957) Indian J Med Sci 11:799
77. Bose BC, Gupta SS, Vijayavergia R, Saifi AQ, Bhatnagar JN (1957) Curr Sci 26:278
78. Chaudhry GR, Sharma VN, Siddiqui S (1951) J Sci Ind Res 10B:48
79. Chaudhry GR, Dhar MM, Nityanand P, Dhar ML (1958) J Sci Ind Res 17B:159
80. Chopra IC, Jamwal KS, Khajuria BN (1986) Indian J Med Res 42:385
81. Mahal AS, Ramu MG, Chaturvedi DD, Thomas KM, Senapati HM, Murthy NNS (1976) Indian J Psychiatr 18:283
82. Bopaiah CP, Pradhan N (2001) Phytother Res 15:153
83. Shukla SD, Jain S, Sharma K, Bhatnagar M (2000) Indian J Exp Biol 38:1007
84. Bhatnagar M, Shukla SD, Bhatnagar R (2005) Herb Pharma Ther 5:21
85. Pauletti PM, Castro-Gamba I, Silva DHS, Young MCM, Tomazela DM, Eberlin MN, Bolzani VS (2003) J Nat Prod 66:1384
86. Watanabe CMH, Wolffram S, Ader P, Rimbach G, Pecker L, Maguire JJ, Schultz PG, Gohil KC (2001) Proc Natl Acad Sci USA 98:6577
87. KarnicLR (1991) Indian Med J 3:1
88. Bhattacharya A, Ghosal S, Bhattacharya SK (2001) J Ethnopharmacol 74:1
89. Tohda C, Kuboyama K, Komatsu K (2000) Neuroreport 11:198
90. Jain S, Shukla SD, Sharma K, Bhatnagar M (2001) Phytother Res 15:544
91. Schliebs R, Leibmann A, Bhattacharya SK, Kumar A, Ghosal S, Bigl V (1997) Neurochem Int 30:181
92. Venturi VM, Piccinin GL, Taddei I (1965) Boll Soc Ital Biol Sper 11:593
93. Wilcock GK, Lilienfield S, Gaens E (2000) BMJ 4:1445
94. Grant WB (1997) AlzDis Rev 2:42
95. Gilani AH, Aziz N, Khan MA, Shaheen F, Jableen Q, Siddiqui BS, Herzig JW (2000) J Ethnopharmacol 71:161
Was this article helpful?
Suffering from Anxiety or Panic Attacks? Discover The Secrets to Stop Attacks in Their Tracks! Your heart is racing so fast and you don’t know why, at least not at first. Then your chest tightens and you feel like you are having a heart attack. All of a sudden, you start sweating and getting jittery.