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Rao, R. Neuroprotective Herbs for Alzheimer’s Disease. Encyclopedia. Available online: https://encyclopedia.pub/entry/9872 (accessed on 08 August 2024).
Rao R. Neuroprotective Herbs for Alzheimer’s Disease. Encyclopedia. Available at: https://encyclopedia.pub/entry/9872. Accessed August 08, 2024.
Rao, Rammohan. "Neuroprotective Herbs for Alzheimer’s Disease" Encyclopedia, https://encyclopedia.pub/entry/9872 (accessed August 08, 2024).
Rao, R. (2021, May 19). Neuroprotective Herbs for Alzheimer’s Disease. In Encyclopedia. https://encyclopedia.pub/entry/9872
Rao, Rammohan. "Neuroprotective Herbs for Alzheimer’s Disease." Encyclopedia. Web. 19 May, 2021.
Neuroprotective Herbs for Alzheimer’s Disease
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Alzheimer’s disease (AD) is a multifactorial, progressive, neurodegenerative disease that is characterized by memory loss, personality changes, and a decline in cognitive function. Medicinal plants and herbal remedies are now gaining more interest as complementary and alternative interventions and are a valuable source for developing drug candidates for AD. Indeed, several scientific studies have described the use of various medicinal plants and their principal phytochemicals for the treatment of AD. 

herbs Alzheimer’s disease neurodegeneration ashwagandha brahmi cat’s claw ginkgo biloba gotu kola lion’s mane saffron shankhpushpi turmeric triphala

1. Introduction

Alzheimer’s disease (AD) is one of the most significant global healthcare problems and is now the third leading cause of death in the United States [1][2][3]. While the etiology is incompletely understood, genetic factors account for the 5 to 10% of cases that are familial Alzheimer’s, with the other 90 to 95% being sporadic. Being heterozygous or homozygous for the ApoE ε4 allele significantly increases the risk of developing Alzheimer’s. Efforts to find a cure for AD have so far been disappointing, and the drugs currently available to treat the disease have limited effectiveness, especially if the disease is in its moderate–severe stage.
The underlying pathology is neuronal degeneration and loss of synapses in the hippocampus, cortex, and subcortical structures. This loss results in gross atrophy of the affected regions, resulting in loss of memory, inability to learn new information, mood swings, executive dysfunction, and an inability to complete activities of daily living (ADLs). Patients in the late–severe stage of AD will require comprehensive care owing to complete loss of memory and the disappearance of their sense of time and place. It is believed that therapeutic intervention that could postpone the onset or progression of AD would dramatically reduce the number of cases over the next 50 years [1][2].
The two prominent pathologic hallmarks of Alzheimer’s disease are (a) extracellular accumulation of β-amyloid deposits and (b) intracellular neurofibrillary tangles (NFT). Accumulated Aβ triggers neurodegeneration, resulting in clinical dementia that is characteristic of AD [4][5][6]. However, the poor correlation of amyloid deposits with cognitive decline in the symptomatic phase of dementia may explain why drug targets to β-amyloid have not succeeded to date [5][6].
Intracellular neurofibrillary tangles (NFTs) are commonly seen in AD brains and represent aberrantly folded and hyperphosphorylated isoforms of the microtubule-associated protein tau [7][8]. Studies reveal that the mutated, aberrantly folded, and hyperphosphorylated tau is less efficient in sustaining microtubule growth and function, resulting in the destabilization of the microtubule network—a hallmark of AD [9]. Attention is now on therapies targeted at tau due to failures in β-amyloid clinical drug trials [7][8][10]. However, the recent failure of drugs targeting tau deposits suggests a lack of accurate understanding of the complex pathophysiology of AD [11]. This demonstrates the need to consider other pathophysiological entities underlying AD, including, but not limited to, autophagy, neuroinflammation, oxidative stress, metal ion toxicity, neurotransmitter excitotoxicity, gut dysbiosis, unfolded protein response, cholesterol metabolism, insulin/glucose dysregulation, and infections [12]. In the face of repeated failures of drug therapies targeting amyloid or tau and the large unmet need for safe and effective AD treatments, it is imperative to pursue alternative therapeutic strategies that address all the above-mentioned pathophysiological entities [13][14].
We reported the first examples of reversal of cognitive decline in AD and pre-AD conditions including mild cognitive impairment (MCI) and subjective cognitive impairment (SCI), using a comprehensive, individualized approach that involves determining the potential contributors to the cognitive decline. Some examples of addressing these potential contributors include: (1) identifying gastrointestinal hyperpermeability, repairing the gut, and optimizing the microbiome; (2) identifying insulin resistance and returning insulin sensitivity; (3) reducing protein glycation; (4) identifying and correcting suboptimal levels of nutrients, hormones, and trophic molecules; (5) identifying and treating pathogens such as Borrelia, Babesia, or Herpes family viruses; and (6) identifying and reducing levels of metallotoxins, organic toxins, or biotoxins through detoxification procedures. This sustained effect of the personalized, precision therapeutic program represents an advantage over monotherapeutics [15]. Included in this individualized, precision program are high-quality herbs or their bioactive compounds directed towards the specific needs of each patient as part of the overall protocol, and these have proven to be very effective.
While herbs and herbal remedies have a long history of traditional use and appear to be safe and effective, they have unfortunately received little scientific attention [16][17][18][19][20]. Numerous plants and their constituents are recommended in traditional practices of medicine to enhance cognitive function and to alleviate other symptoms of AD, including poor cognition, memory loss, and depression. A single herb or a mixture of herbs is normally recommended depending upon the complexity of the condition. The rationale is that the bioactive principles present in the herb not only act synergistically but may also modulate the activity of other constituents from the same plant or other plant species [20][21][22]. This approach has been used in Ayurveda, traditional Chinese medicine (TCM), and Native Americans’ system of medicine, where a single herb or a combination of two or more herbs is commonly prescribed for any specific disease [16][17][18][19][23] (Table 1).
Table 1. Neuroprotective herbs for the management of AD have a wide gamut of physiological actions. Listed below are the neurotherapeutic properties of these herbs that ultimately enhance memory and restore normal cognitive functions.

Herb

Study Type

Function/Outcome Measure

Reference

Ashwagandha

(Withania somnifera)

in vitro, in vivo,

clinical studies

antioxidant, anti-inflammatory, blocks Aβ production, inhibits neural cell death, dendrite extension, neurite outgrowth and restores synaptic function, neural regeneration, reverses mitochondrial dysfunction, improves auditory–verbal working memory, executive function, processing speed, and social cognition in patients

[20][23][24][25][26][27][28][29]

Brahmi

(Bacopa monnieri)

in vitro, in vivo,

clinical studies

antioxidant, anti-inflammatory, improves memory, attention, executive function, blocks Aβ production, inhibits neural cell death, delays brain aging, improves cardiac function

[30][31][32][33][34][35][36][37]

Cat’s claw

(Uncaria tomentosa)

in vitro, in vivo,

pre-clinical

studies

anti-inflammatory, antioxidant, inhibits plaques and tangles,

reduces gliosis, improves memory

[38][39][40][41][42][43][44][45]

Ginkgo biloba

in vitro, pre-clinical,

clinical studies

antioxidant, improves mitochondrial function, stimulates cerebral blood flow, blocks neural cell death, stimulates neurogenesis

[46][47][48][49][50]

Gotu kola

(Centella asiatica)

in vitro, in vivo,

clinical studies

neuroceutical, cogniceutical,

reduces oxidative stress, Aβ levels, and apoptosis, promotes dendritic growth and

mitochondrial health, improves mood and memory

[51][52][53][54][55][56][57][58]

Lion’s mane

(Hericium erinaceus)

in vitro, in vivo,

pre-clinical and

clinical studies

neuroprotective, improves cognition, anti-inflammatory, blocks Aβ production, stimulates neurotransmission and neurite outgrowth

[59][60][61][62][63]

Saffron

(Crocus sativus)

in vitro, in vivo,

clinical studies

antioxidant, anti-amyloidogenic,

anti-inflammatory, antidepressant,

immunomodulation,

neuroprotection

[64][65][66]

Shankhpushpi

(Convolvulus pluricaulis)

in vitro, in vivo,

pre-clinical studies

promotes cognitive function,

slows brain aging,

antioxidant, anti-inflammatory

[33][36][67][68][69][70].

Triphala

(Emblica officinalis,

Terminalia bellerica, and Terminalia chebula)

in vitro, in vivo,

pre-clinical and clinical studies

antioxidant, anti-inflammatory, immunomodulation, prevents dental caries, antibacterial,

antiparasitic, reverses metabolic disturbances

[71][72][73][74][75][76].

Turmeric

(Curcuma longa)

in vitro, in vivo,

pre-clinical and clinical studies

antioxidant, anti-inflammatory, antimicrobial, blocks Aβ production, inhibits neural cell death

[77][78][79][80][81][82][83][84][85].

It is hoped that the historical knowledge base of traditional systems of medicine, coupled with combinatorial sciences and high-throughput screening techniques, will improve the ease with which herbal products and formulations can be used in the drug development process to provide new functional leads for AD.

2. Other Medicinal Plants for AD

There are several other medicinal plants that have a role in the prevention or treatment of AD. However, in vitro or in vivo studies pertaining to their role in AD are very limited, the majority of the data are from observational studies, and there are no studies to support their role in preventing dementia. These plants include vacha (Acorus calamus), guduchi (Tinospora cordifolia), guggul (Commiphora wightii), jatamansi (Nardostachys jatamansi), jyotismati (Celastrus paniculatus), rosemary (Rosmarinus officinalis), Green tea (Camellia sinensis), St john’s wort (Hypericum perforatum), sage (Salvia spp), Rhodiola rosea, Moringa oleifera, shilajit, and lemon balm.

3. Administration of Herbs

The biggest challenge to drug delivery into the brain is circumventing the BBB, which prevents the entry of numerous potential therapeutic agents. While oral administration of the herbs is a common route of administration, there are no clear studies to demonstrate whether the herbal components have access to the CNS from the systemic circulation. Intranasal administration (INA) is non-invasive, rapid, bypasses the BBB, and directly targets the CNS [17][86][87][88][89][90]. Using this route of delivery, herbs in the form of dry powders or medicated oils are directly administered. Medicated oils may contain a mix of lipophilic and lipid-soluble molecules to ensure the synergistic interaction between different constituents in the herb. The benefits of INA include minimizing the side effects associated with systemic administration, avoidance of brain injury, and overcoming the need for implanting delivery devices [91]. Using this technique, researchers have treated memory losses in transgenic mouse models of AD [92]. While INA may be of great value, several contradictory findings in research studies limit its clinical value [92][93]. Though an attractive strategy in traditional medicinal systems for CNS conditions, there are not many clinical studies to support the use of INS for herbal delivery.
Another method of herbal administration involves the application of a medicated oil on the body and massaging the areas with gentle or deep hand movements. Massage reduces the levels of stress-related hormones and also triggers rapid cerebral blood flow [17][94][95][96][97]. Yet another mode of administration is a transcranial application of medicated oils so that the herbal extracts in the oil are in contact with the cranium or the frontal regions of the brain [17][98][99]. Recent studies point to the role of the endothelial cells lining the CNS capillaries in facilitating the entry of the solutes from the oil into the frontal lobe and prefrontal cortex [17][98][99][100].

References

  1. 2020 Alzheimer’s disease facts and figures. Alzheimers Dement. 2020.
  2. El-Hayek, Y.H.; Wiley, R.E.; Khoury, C.P.; Daya, R.P.; Ballard, C.; Evans, A.R.; Karran, M.; Molinuevo, J.L.; Norton, M.; Atri, A. Tip of the Iceberg: Assessing the Global Socioeconomic Costs of Alzheimer’s Disease and Related Dementias and Strategic Implications for Stakeholders. J. Alzheimers Dis. 2019, 70, 323–341.
  3. James, B.D.; Leurgans, S.E.; Hebert, L.E.; Scherr, P.A.; Yaffe, K.; Bennett, D.A. Contribution of Alzheimer disease to mortality in the United States. Neurology 2014, 82, 1045–1050.
  4. Selkoe, D.J.; Hardy, J. The amyloid hypothesis of Alzheimer’s disease at 25 years. EMBO Mol. Med. 2016, 8, 595–608.
  5. Murphy, M.P.; LeVine, H., 3rd. Alzheimer’s disease and the amyloid-beta peptide. J. Alzheimers Dis. 2010, 19, 311–323.
  6. Prasansuklab, A.; Tencomnao, T. Amyloidosis in Alzheimer’s Disease: The Toxicity of Amyloid Beta (A beta), Mechanisms of Its Accumulation and Implications of Medicinal Plants for Therapy. Evid. Based Complement Alternat. Med. 2013, 2013, 413808.
  7. Iqbal, K.; Liu, F.; Gong, C.X. Tau and neurodegenerative disease: The story so far. Nat. Rev. Neurol. 2016, 12, 15–27.
  8. Busche, M.A.; Hyman, B.T. Synergy between amyloid-beta and tau in Alzheimer’s disease. Nat. Neurosci. 2020, 23, 1183–1193.
  9. Iqbal, K.; Gong, C.X.; Liu, F. Microtubule-associated protein tau as a therapeutic target in Alzheimer’s disease. Expert Opin. Ther. Targets 2014, 18, 307–318.
  10. Congdon, E.E.; Sigurdsson, E.M. Tau-targeting therapies for Alzheimer disease. Nat. Rev. Neurol. 2018, 14, 399–415.
  11. Mehta, D.; Jackson, R.; Paul, G.; Shi, J.; Sabbagh, M. Why do trials for Alzheimer’s disease drugs keep failing? A discontinued drug perspective for 2010-2015. Expert Opin. Investig. Drugs 2017, 26, 735–739.
  12. Calabro, M.; Rinaldi, C.; Santoro, G.; Crisafulli, C. The biological pathways of Alzheimer disease: A review. AIMS Neurosci. 2021, 8, 86–132.
  13. Folch, J.; Petrov, D.; Ettcheto, M.; Abad, S.; Sánchez-López, E.; García, M.L.; Olloquequi, J.; Beas-Zarate, C.; Auladell, C.; Camins, A. Current Research Therapeutic Strategies for Alzheimer’s Disease Treatment. Neural. Plast. 2016, 2016, 8501693.
  14. Ngandu, T.; Lehtisalo, J.; Solomon, A.; Levälahti, E.; Ahtiluoto, S.; Antikainen, R.; Bäckman, L.; Hänninen, T.; Jula, A.; Laatikainen, T.; et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): A randomised controlled trial. Lancet 2015, 385, 2255–2263.
  15. Bredesen, D.E.; Sharlin, K.; Jenkins, D.; Okuno, M.; Youngberg, W.; Cohen, S.H.; Stefani, A.; Brown, R.L.; Conger, S.; Tanio, C.; et al. Reversal of Cognitive Decline: 100 Patients. J. Alzheimer’s Dis. Parkinsonism 2018, 8, 1–6.
  16. Patwardhan, B.; Bodeker, G. Ayurvedic genomics: Establishing a genetic basis for mind-body typologies. J. Altern. Complement Med. 2008, 14, 571–576.
  17. Rao, R.V.; Descamps, O.; John, V.; Bredesen, D.E. Ayurvedic medicinal plants for Alzheimer’s disease: A review. Alzheimers Res. Ther. 2012, 4, 22.
  18. Parasuraman, S.; Thing, G.S.; Dhanaraj, S.A. Polyherbal formulation: Concept of ayurveda. Pharmacogn. Rev. 2014, 8, 73–80.
  19. Barkat, M.A.; Goyal, A.; Barkat, H.A.; Salauddin, M.; Pottoo, F.H.; Anwer, E.T. Herbal Medicine: Clinical Perspective & Regulatory Status. Comb. Chem. High Throughput Screen. 2020.
  20. Yarnell, K.A.a.E. Alzheimer’s Disease-Part 2—A Botanical Treatment Plan. Altern. Complementary Ther. 2004, 10, 67–72.
  21. Wagner, H.; Ulrich-Merzenich, G. Synergy research: Approaching a new generation of phytopharmaceuticals. Phytomedicine 2009, 16, 97–110.
  22. Rasoanaivo, P.; Wright, C.W.; Willcox, M.L.; Gilbert, B. Whole plant extracts versus single compounds for the treatment of malaria: Synergy and positive interactions. Malar. J. 2011, 10 (Suppl. 1), S4.
  23. Howes, M.J.; Houghton, P.J. Plants used in Chinese and Indian traditional medicine for improvement of memory and cognitive function. Pharmacol. Biochem. Behav. 2003, 75, 513–527.
  24. Pratte, M.A.; Nanavati, K.B.; Young, V.; Morley, C.P. An alternative treatment for anxiety: A systematic review of human trial results reported for the Ayurvedic herb ashwagandha (Withania somnifera). J. Altern. Complement Med. 2014, 20, 901–908.
  25. Pingali, U.; Pilli, R.; Fatima, N. Effect of standardized aqueous extract of Withania somnifera on tests of cognitive and psychomotor performance in healthy human participants. Pharmacogn. Res. 2014, 6, 12–18.
  26. Namdeo, A.G.; Ingawale, D.K. Ashwagandha: Advances in plant biotechnological approaches for propagation and production of bioactive compounds. J. Ethnopharmacol. 2020, 271, 113709.
  27. Chengappa, K.N.; Bowie, C.R.; Schlicht, P.J.; Fleet, D.; Brar, J.S.; Jindal, R. Randomized placebo-controlled adjunctive study of an extract of Withania somnifera for cognitive dysfunction in bipolar disorder. J. Clin. Psychiatry 2013, 74, 1076–1083.
  28. Zahiruddin, S.; Basist, P.; Parveen, A.; Parveen, R.; Khan, W.; Ahmad, S. Ashwagandha in brain disorders: A review of recent developments. J. Ethnopharmacol. 2020, 257, 112876.
  29. Kuboyama, T.; Tohda, C.; Zhao, J.; Nakamura, N.; Hattori, M.; Komatsu, K. Axon- or dendrite-predominant outgrowth induced by constituents from Ashwagandha. Neuroreport 2002, 13, 1715–1720.
  30. Stough, C.; Lloyd, J.; Clarke, J.; A Downey, L.; Hutchison, C.W.; Rodgers, T.; Nathan, P.J. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology 2001, 156, 481–484.
  31. Benson, S.; Downey, L.A.; Stough, C.; Wetherell, M.; Zangara, A.; Scholey, A. An acute, double-blind, placebo-controlled cross-over study of 320 mg and 640 mg doses of Bacopa monnieri (CDRI 08) on multitasking stress reactivity and mood. Phytother. Res. 2014, 28, 551–559.
  32. Sadhu, A.; Upadhyay, P.; Agrawal, A.; Ilango, K.; Karmakar, D.; Singh, G.P.I.; Dubey, G.P. Management of cognitive determinants in senile dementia of Alzheimer’s type: Therapeutic potential of a novel polyherbal drug product. Clin. Drug Investig. 2014, 34, 857–869.
  33. Farooqui, A.A.; Farooqui, T.; Madan, A.; Ong, J.H.; Ong, W.Y. Ayurvedic Medicine for the Treatment of Dementia: Mechanistic Aspects. Evid. Based Complement Alternat. Med. 2018, 2018, 2481076.
  34. Aguiar, S.; Borowski, T. Neuropharmacological review of the nootropic herb Bacopa monnieri. Rejuvenation Res. 2013, 16, 313–326.
  35. Uabundit, N.; Wattanathorn, J.; Mucimapura, S.; Ingkaninan, K. Cognitive enhancement and neuroprotective effects of Bacopa monnieri in Alzheimer’s disease model. J. Ethnopharmacol. 2010, 127, 26–31.
  36. Kumar, V. Potential medicinal plants for CNS disorders: An overview. Phytother. Res. 2006, 20, 1023–1035.
  37. Raghav, S.; Singh, H.; Dalal, P.K.; Srivastava, J.S.; Asthana, O.P. Randomized controlled trial of standardized Bacopa monniera extract in age-associated memory impairment. Indian J. Psychiatry 2006, 48, 238–242.
  38. Batiha, G.E.-S.; Beshbishy, A.M.; Wasef, L.; Elewa, Y.H.A.; El-Hack, M.E.A.; Taha, A.E.; Al-Sagheer, A.A.; Devkota, H.P.; Tufarelli, V. Uncaria tomentosa (Willd. ex Schult.) DC.: A Review on Chemical Constituents and Biological Activities. Appl. Sci. 2020, 10, 2668.
  39. Heitzman, M.E.; Neto, C.C.; Winiarz, E.; Vaisberg, A.J.; Hammond, G.B. Ethnobotany, phytochemistry and pharmacology of Uncaria (Rubiaceae). Phytochmistry 2005, 66, 5–29.
  40. Sandoval, M.; Okuhama, N.N.; Zhang, X.J.; Condezo, L.A.; Lao, J.; Angeles, F.M.; Musah, R.A.; Bobrowski, P.; Miller, M.J. Anti-inflammatory and antioxidant activities of cat’s claw (Uncaria tomentosa and Uncaria guianensis) are independent of their alkaloid content. Phytomedicine 2002, 9, 325–337.
  41. Yatoo, M.I.; Gopalakrishnan, A.; Saxena, A.; Parray, O.R.; Tufani, N.A.; Chakraborty, S.; Tiwari, R.; Dhama, K.; Iqbal, H.M. Anti-Inflammatory Drugs and Herbs with Special Emphasis on Herbal Medicines for Countering Inflammatory Diseases and Disorders-A Review. Recent Pat. Inflamm. Allergy Drug Discov. 2018, 12, 39–58.
  42. Mur, E.; Hartig, F.; Eibl, G.; Schirmer, M. Randomized double blind trial of an extract from the pentacyclic alkaloid-chemotype of Uncaria tomentosa for the treatment of rheumatoid arthritis. J. Rheumatol. 2002, 29, 678–681.
  43. Kirschner, D.A.; Gross, A.A.R.; Hidalgo, M.M.; Inouye, H.; Gleason, K.A.; Abdelsayed, G.A.; Castillo, G.M.; Snow, A.D.; Pozo-Ramajo, A.; Petty, S.A.; et al. Fiber diffraction as a screen for amyloid inhibitors. Curr. Alzheimer Res. 2008, 5, 288–307.
  44. Snow, A.D.; Castillo, G.M.; Nguyen, B.P.; Choi, P.Y.; Cummings, J.A.; Cam, J.; Hu, Q.; Lake, T.; Pan, W.; Kastin, A.J.; et al. The Amazon rain forest plant Uncaria tomentosa (cat’s claw) and its specific proanthocyanidin constituents are potent inhibitors and reducers of both brain plaques and tangles. Sci. Rep. 2019, 9, 561.
  45. Hardin, S.R. Cat’s claw: An Amazonian vine decreases inflammation in osteoarthritis. Complement Ther. Clin. Pract. 2007, 13, 25–28.
  46. Yasuno, F.; Tanimukai, S.; Sasaki, M.; Ikejima, C.; Yamashita, F.; Kodama, C.; Mizukami, K.; Asada, T. Combination of antioxidant supplements improved cognitive function in the elderly. J. Alzheimers Dis. 2012, 32, 895–903.
  47. Osman, N.M.; Amer, A.S.; Abdelwahab, S. Effects of Ginko biloba leaf extract on the neurogenesis of the hippocampal dentate gyrus in the elderly mice. Anat. Sci. Int. 2016, 91, 280–289.
  48. Smith, J.V.; Luo, Y. Studies on molecular mechanisms of Ginkgo biloba extract. Appl. Microbiol. Biotechnol. 2004, 64, 465–472.
  49. Ramassamy, C.; Longpre, F.; Christen, Y. Ginkgo biloba extract (EGb 761) in Alzheimer’s disease: Is there any evidence? Curr. Alzheimer Res. 2007, 4, 253–262.
  50. Mahadevan, S.; Park, Y. Multifaceted therapeutic benefits of Ginkgo biloba L.: Chemistry, efficacy, safety, and uses. J. Food Sci. 2008, 73, R14–R19.
  51. Puttarak, P.; Dilokthornsakul, P.; Saokaew, S.; Dhippayom, T.; Kongkaew, C.; Sruamsiri, R.; Chuthaputti, A.; Chaiyakunapruk, N. Effects of Centella asiatica (L.) Urb. on cognitive function and mood related outcomes: A Systematic Review and Meta-analysis. Sci. Rep. 2017, 7, 10646.
  52. Wattanathorn, J.; Mator, L.; Muchimapura, S.; Tongun, T.; Pasuriwong, O.; Piyawatkul, N.; Yimtae, K.; Sripanidkulchai, B.; Singkhoraard, J. Positive modulation of cognition and mood in the healthy elderly volunteer following the administration of Centella asiatica. J. Ethnopharmacol. 2008, 116, 325–332.
  53. Soumyanath, A.; Zhong, Y.P.; Henson, E.; Wadsworth, T.; Bishop, J.; Gold, B.G.; Quinn, J.F. Centella asiatica Extract Improves Behavioral Deficits in a Mouse Model of Alzheimer’s Disease: Investigation of a Possible Mechanism of Action. Int. J. Alzheimers Dis. 2012, 2012, 381974.
  54. Mehla, J.; Gupta, P.; Pahuja, M.; Diwan, D.; Diksha, D. Indian Medicinal Herbs and Formulations for Alzheimer’s Disease, from Traditional Knowledge to Scientific Assessment. Brain Sci. 2020, 10, 964.
  55. Cervenka, F.; Jahodar, L. [Plant metabolites as nootropics and cognitives]. Ceska Slov. Farm. 2006, 55, 219–229.
  56. Shinomol, G.K.; Muralidhara; Bharath, M.M. Exploring the Role of “Brahmi” (Bocopa monnieri and Centella asiatica) in Brain Function and Therapy. Recent Pat. Endocr. Metab. Immune Drug Discov. 2011, 5, 33–49.
  57. Orhan, I.E. Centella asiatica (L.) Urban: From Traditional Medicine to Modern Medicine with Neuroprotective Potential. Evid. Based Complement Alternat. Med. 2012, 2012, 946259.
  58. Da Rocha, M.D.; Viegas, F.P.; Campos, H.C.; Nicastro, P.C.; Fossaluzza, P.C.; Fraga, C.A.; Barreiro, E.J.; Viegas, C., Jr. The role of natural products in the discovery of new drug candidates for the treatment of neurodegenerative disorders II: Alzheimer’s disease. CNS Neurol. Disord. Drug Targets 2011, 10, 251–270.
  59. Venturella, G.; Ferraro, V.; Cirlincione, F.; Gargano, M.L. Medicinal Mushrooms: Bioactive Compounds, Use, and Clinical Trials. Int. J. Mol. Sci. 2021, 22, 634.
  60. Spelman, K.; Sutherland, E.; Bagade, A. Neurological activity of Lion’s mane (Hericium erinaceus). J. Restor. Med. 2017, 6, 16–26.
  61. Tsai-Teng, T.; Chin-Chu, C.; Li-Ya, L.; Wan-Ping, C.; Chung-Kuang, L.; Chien-Chang, S.; Chi-Ying, H.F.; Chien-Chih, C.; Shiao, Y.J. Erinacine A-enriched Hericium erinaceus mycelium ameliorates Alzheimer’s disease-related pathologies in APPswe/PS1dE9 transgenic mice. J. Biomed. Sci. 2016, 23, 49.
  62. Zhang, C.C.; Cao, C.Y.; Kubo, M.; Harada, K.; Yan, X.T.; Fukuyama, Y.; Gao, J.M. Chemical Constituents from Hericium erinaceus Promote Neuronal Survival and Potentiate Neurite Outgrowth via the TrkA/Erk1/2 Pathway. Int. J. Mol. Sci. 2017, 18, 1659.
  63. Tzeng, T.-T.; Chen, C.-C.; Chen, C.-C.; Tsay, H.-J.; Lee, L.-Y.; Chen, W.-P.; Shen, C.-C.; Shiao, Y.-J. The Cyanthin Diterpenoid and Sesterterpene Constituents of Hericium erinaceus Mycelium Ameliorate Alzheimer’s Disease-Related Pathologies in APP/PS1 Transgenic Mice. Int. J. Mol. Sci. 2018, 19, 598.
  64. Adalier, N.; Parker, H. Vitamin E, Turmeric and Saffron in Treatment of Alzheimer’s Disease. Antioxidants 2016, 5, 40.
  65. Khazdair, M.R.; Boskabady, M.H.; Hosseini, M.; Rezaee, R.; Tsatsakis, A.M. The effects of Crocus sativus (saffron) and its constituents on nervous system: A review. Avicenna J. Phytomed. 2015, 5, 376–391.
  66. Gohari, A.R.; Saeidnia, S.; Mahmoodabadi, M.K. An overview on saffron, phytochemicals, and medicinal properties. Pharmacogn. Rev. 2013, 7, 61–66.
  67. Mukherjee, P.K.; Kumar, V.; Kumar, N.S.; Heinrich, M. The Ayurvedic medicine Clitoria ternatea--from traditional use to scientific assessment. J. Ethnopharmacol. 2008, 120, 291–301.
  68. Malik, J.; Karan, M.; Vasisht, K. Nootropic, anxiolytic and CNS-depressant studies on different plant sources of shankhpushpi. Pharm. Biol. 2011, 49, 1234–1242.
  69. Sethiya, N.K.; Nahata, A.; Mishra, S.H.; Dixit, V.K. An update on Shankhpushpi, a cognition-boosting Ayurvedic medicine. Zhong Xi Yi Jie He Xue Bao 2009, 7, 1001–1022.
  70. Balkrishna, A.; Thakur, P.; Varshney, A. Phytochemical Profile, Pharmacological Attributes and Medicinal Properties of Convolvulus prostratus-A Cognitive Enhancer Herb for the Management of Neurodegenerative Etiologies. Front. Pharmacol. 2020, 11, 171.
  71. Peterson, C.T.; Denniston, K.; Chopra, D. Therapeutic Uses of Triphala in Ayurvedic Medicine. J. Altern. Complement Med. 2017, 23, 607–614.
  72. Baliga, M.S. Triphala, Ayurvedic formulation for treating and preventing cancer: A review. J. Altern. Complement Med. 2010, 16, 1301–1308.
  73. Chouhan, B.; Kumawat, R.C.; Kotecha, M.; Ramamurthy, A.; Nathani, S. Triphala: A comprehensive Ayurvedic review. Int. J. Res. Ayurveda Pharm. 2013, 4, 612–617.
  74. Sabu, M.C.; Kuttan, R. Anti-diabetic activity of medicinal plants and its relationship with their antioxidant property. J. Ethnopharmacol. 2002, 81, 155–160.
  75. Baratakke, S.U.; Raju, R.; Kadanakuppe, S.; Savanur, N.R.; Gubbihal, R.; Kousalaya, P.S. Efficacy of triphala extract and chlorhexidine mouth rinse against plaque accumulation and gingival inflammation among female undergraduates: A randomized controlled trial. Indian J. Dent. Res. 2017, 28, 49–54.
  76. Peterson, C.T.; Sharma, V.; Uchitel, S.; Denniston, K.; Chopra, D.; Mills, P.J.; Peterson, S.N. Prebiotic Potential of Herbal Medicines Used in Digestive Health and Disease. J. Altern. Complement. Med. 2018, 24, 656–665.
  77. Begum, A.N.; Jones, M.R.; Lim, G.P.; Morihara, T.; Kim, P.; Heath, D.D.; Rock, C.L.; Pruitt, M.A.; Yang, F.; Hudspeth, B.; et al. Curcumin structure-function, bioavailability, and efficacy in models of neuroinflammation and Alzheimer’s disease. J. Pharmacol. Exp. Ther. 2008, 326, 196–208.
  78. Lim, G.P.; Chu, T.; Yang, F.; Beech, W.; Frautschy, S.A.; Cole, G.M. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J. Neurosci. 2001, 21, 8370–8377.
  79. Sharifi-Rad, J.; El Rayess, Y.; Rizk, A.A.; Sadaka, C.; Zgheib, R.; Zam, W.; Sestito, S.; Rapposelli, S.; Neffe-Skocińska, K.; Zielińska, D.; et al. Turmeric and Its Major Compound Curcumin on Health: Bioactive Effects and Safety Profiles for Food, Pharmaceutical, Biotechnological and Medicinal Applications. Front. Pharmacol. 2020, 11, 01021.
  80. Chainani-Wu, N. Safety and anti-inflammatory activity of curcumin: A component of tumeric (Curcuma longa). J. Altern. Complement Med. 2003, 9, 161–168.
  81. Aggarwal, B.B.; Sundaram, C.; Malani, N.; Ichikawa, H. Curcumin: The Indian solid gold. Adv. Exp. Med. Biol. 2007, 595, 1–75.
  82. Breitner, J.C.; Welsh, K.A.; Helms, M.J.; Gaskell, P.C.; Gau, B.A.; Roses, A.D.; Pericak-Vance, M.A.; Saunders, A.M. Delayed onset of Alzheimer’s disease with nonsteroidal anti-inflammatory and histamine H2 blocking drugs. Neurobiol. Aging 1995, 16, 523–530.
  83. Parachikova, A.; Green, K.N.; Hendrix, C.; LaFerla, F.M. Formulation of a medical food cocktail for Alzheimer’s disease: Beneficial effects on cognition and neuropathology in a mouse model of the disease. PLoS ONE 2010, 5, e14015.
  84. Hewlings, S.J.; Kalman, D.S. Curcumin: A Review of Its Effects on Human Health. Foods 2017, 6, 92.
  85. Voulgaropoulou, S.D.; van Amelsvoort, T.; Prickaerts, J.; Vingerhoets, C. The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies. Brain Res. 2019, 1725, 146476.
  86. Pires, A.; Fortuna, A.; Alves, G.; Falcao, A. Intranasal drug delivery: How, why and what for? J. Pharm. Pharm. Sci. 2009, 12, 288–311.
  87. Turker, S.; Onur, E.; Ozer, Y. Nasal route and drug delivery systems. Pharm. World Sci. 2004, 26, 137–142.
  88. Illum, L. Nasal drug delivery--possibilities, problems and solutions. J. Control Release 2003, 87, 187–198.
  89. Craft, S.; Baker, L.D.; Montine, T.J.; Minoshima, S.; Watson, G.S.; Claxton, A.; Arbuckle, M.; Callaghan, M.; Tsai, E.; Plymate, S.R.; et al. Intranasal Insulin Therapy for Alzheimer Disease and Amnestic Mild Cognitive Impairment: A Pilot Clinical Trial. Arch. Neurol. 2011.
  90. Dhuria, S.V.; Hanson, L.R.; Frey, W.H., 2nd. Intranasal delivery to the central nervous system: Mechanisms and experimental considerations. J. Pharm. Sci. 2010, 99, 1654–1673.
  91. Hanson, L.R.; Frey, W.H., 2nd. Intranasal delivery bypasses the blood-brain barrier to target therapeutic agents to the central nervous system and treat neurodegenerative disease. BMC Neurosci. 2008, 9 (Suppl. 3), S5.
  92. Miyake, M.M.; Bleier, B.S. The blood-brain barrier and nasal drug delivery to the central nervous system. Am. J. Rhinol. Allergy 2015, 29, 124–127.
  93. Erdo, F.; Bors, L.A.; Farkas, D.; Bajza, A.; Gizurarson, S. Evaluation of intranasal delivery route of drug administration for brain targeting. Brain Res. Bull. 2018, 143, 155–170.
  94. Rapaport, M.H.; Schettler, P.; Bresee, C. A Preliminary Study of the Effects of a Single Session of Swedish Massage on Hypothalamic-Pituitary-Adrenal and Immune Function in Normal Individuals. J. Altern. Complement Med. 2010.
  95. Buckle, J.; Newberg, A.; Wintering, N.; Hutton, E.; Lido, C.; Farrar, J.T. Measurement of regional cerebral blood flow associated with the M technique-light massage therapy: A case series and longitudinal study using SPECT. J. Altern. Complement Med. 2008, 14, 903–910.
  96. Keir, S.T. Effect of massage therapy on stress levels and quality of life in brain tumor patients--observations from a pilot study. Support Care Cancer. 2011, 19, 711–715.
  97. Ouchi, Y.; Kanno, T.; Okada, H.; Yoshikawa, E.; Shinke, T.; Nagasawa, S.; Minoda, K.; Doi, H. Changes in cerebral blood flow under the prone condition with and without massage. Neurosci. Lett. 2006, 407, 131–135.
  98. Uebaba, K.; Xu, F.H.; Ogawa, H.; Tatsuse, T.; Wang, B.H.; Hisajima, T.; Venkatraman, S. Psychoneuroimmunologic effects of Ayurvedic oil-dripping treatment. J. Altern. Complement Med. 2008, 14, 1189–1198.
  99. Xu, F.; Uebaba, K.; Ogawa, H.; Tatsuse, T.; Wang, B.H.; Hisajima, T.; Venkatraman, S. Pharmaco-physio-psychologic effect of Ayurvedic oil-dripping treatment using an essential oil from Lavendula angustifolia. J. Altern. Complement Med. 2008, 14, 947–956.
  100. Bredesen, D.E.; Rao, R.V. Ayurvedic Profiling of Alzheimer’s Disease. Altern. Ther. Health Med. 2017, 23, 46–50.
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