Noten, vette vis, bessen, kruiden (salie, citroenmelisse, geelwortel) en verrassend genoeg ook koffie en chocolade kunnen helpen bij dementie en de ziekte van Alzheimer.
Bij de ziekte van Alzheimer hebben we te maken met een globale achteruitgang van het functioneren van delen van de hersenen, die nodig zijn voor oriëntatie geheugen en verwante vormen van gedrag. Wandelen, goed dieet (vis) en ook kruiden kunnen ondersteunend werken. Kortgeleden werd een mooi overzichtsartikel over de waarde van kruiden bij Alzheimer gepubliceerd, waaruit blijkt dat Melissa officinalis (oertinctuur 3 maal daags 20 druppels) en Ginkgo een positieve bijdrage kunnen leveren bij het ondersteunen van geheugenproblemen. Ook Salvia en enkele Chinese kruiden kunnen helpen bij symptomen van de ziekte van Alzheimer. Zie verder referenties overzicht
Bij deze aandoening is het zo dat zich een bepaald eiwit in de hersenen gaat afzetten: het bèta-amyloïd. De overproductie van dit ontstekingseiwit, dat zich neerzet onder de vorming van “seniele plaques” in de hersenen, is uiteraard nefast voor het functioneren en het onderling communiceren van zenuwcellen. Uiteindelijk sterven de al slecht werkende zenuwcellen af en leidt de ziekte in verschillende stadia tot totale dementie en volledige afhankelijkheid.
Nu zijn bepaalde mensen wel gevoeliger voor het ontwikkelen van de ziekte van Alzheimer: dragers van het zogenaamde “apo-E-gen”. Maar dat neemt niet weg dat tot de hoofdoorzaken van deze ziekte behoren: een gebrek aan essentiële vetzuren (zoals DHA), aan antioxidanten (zoals vitamine E en co-enzyme Q10), aan vitamines B (vooral foliumzuur) en een accumulatie van toxische stoffen in de hersenen (zoals aluminium).
Ook de granaatappel blijkt door zijn antioxidanten het ontstekingsproces met afzetting van bèta-amyloïd dermate te kunnen afremmen dat het verloop van de ziekte van Alzheimer merkbaar kan vertraagd worden. Tot 50 %, geeft een recent onderzoek op muizen aangetoond. Vooral ellaginezuur en punicalagine remmen een enzym af (bètasecretase of BACE1), dat normaal de afzetting van bèta-amyloïd in de hand werkt. Samen met voedingssupplementen zoals het essentiële omega-3-vetzuur DHA (docosahexaeenzuur), een curcumapreparaat met goed opneembare curcuminoïden, de uit lecithine gehaalde zenuwvoedende stoffen zoals fosfatidylcholine en fosfatidylserine en het vitamine B-complex (vnml. B6, B9 en B12), is de granaatappel dus een veelbelovende maatregel, die kan worden ingezet om die vreselijke ziekte te voorkomen en af te remmen.
The best thing you can do to keep your brain working the way you want it to: exercise, and eat right. "Nutrition is very, very important to brain health," says Paul Nussbaum, Ph.D., a clinical neuropsychologist and member of scientific advisory board for the Alzheimer’s Foundation of America. "Surprisingly, the brain is made up of 60% fat--it’s the fattest part of our body--and that fat insulates the nerve tracks. Without that fat we slow down mentally," Dr. Nussbaum says.
The crucial thing to know: The kinds of fats and foods you eat, can have a real impact on the health of your brain. Trans fats and sugar aren't great for your brain health. What foods are good and can reduce your risk of Alzheimer’s? Consider eating these good-for-your-brain foods:
1. Walnuts (and almonds, pecans, hazelnuts)
Walnuts might be small in size, but they pack a big nutritional punch. They are filled with Omega-3 fatty acids, the good kind of fat your brain needs. A study from the New York State Institute for Basic Research in Developmental Disabilities found that mice given a diet including walnuts showed improvement in memory and motor coordination. Walnuts also contain vitamin E and flavonoids, which can help protect the brain.
2. Salmon (and mackerel, sardines, other fatty fish)
Also high in Omega-3s, fatty fish like salmon can lower blood levels of beta-amyloid, a protein thought to play a role in Alzheimer’s. A Columbia University study found that the more Omega-3 fatty acids a person eats, the lower their blood beta-amyloid levels. Dr. Nussbaum suggests eating 8 oz. of fish per week--fresh fish is best, but you can also talk to your doctor about taking a fish oil supplement.
3. Berries
“Antioxidants are like taking out the broom in the spring and sweeping the garage,” Dr. Nussbaum says. “Antioxidants are the body’s broom.” Berries contain polyphenols, a type of antioxidant which helps stop inflammation and allows brain cells to work better. A Tufts University study found that berries can reverse slow-downs in the brain’s ability to process information.
“You can’t go wrong if a food has the word ‘berry’ in the name,” says Dr. Nussbaum. “Strawberries, blueberries, cranberries-- they’re all good for your brain.”
4. Spinach (and kale, other leafy greens)
Full of antioxidants and fiber, leafy greens should be a diet staple. In a national study, women in their 60s who ate more leafy vegetables over time did better than their non-greens-eating counterparts on memory, verbal, and other tests. And new studies show that high levels of vitamin C, which is found in spinach, may help with dementia prevention.
5. Turmeric
Break out the curry! A host of studies have shown that turmeric, the spice used in curries, and its main active component curcumin, can help prevent Alzheimer's. In one such study, researchers from UCLA found that vitamin D3, taken with curcumin, may help the immune system to get rid of the amino acids that form the plaque in the brain that's associated with Alzheimer’s Disease. So the next time you cook, incorporate this healthy spice.
6. Coffee
Now you don’t have to feel guilty about pouring yourself another cup. Researchers from the University of South Florida and University of Miami found that people older than 65 who drank three cups of coffee a day (i.e. had higher blood levels of caffeine) developed Alzheimer's disease two to four years later than their counterparts with lower caffeine levels, and that caffeine had a positive impact even in older adults who were already showing early signs of Alzheimer's.
7. Chocolate
If you haven’t already switched from milk chocolate to dark, now you have one more reason to. Compelling research already shows that dark chocolate, which contains flavonoids (a plant compound that helps with the body’s circulation), can help combat heart disease, but flavonoids may also help slow down the effects of dementia. In an Italian study, older adults who had mild symptoms of dementia drank cocoa with high, medium and low amounts of flavonoids. Those who consumed high amounts outperformed those who consumed low doses on cognitive tests.
And a study is currently underway by the National Institute on Aging to see whether resveratrol, a compound found in chocolate, red wine, and grapes, can prevent dementia. One tip: A healthy choice is dark chocolate that has a 70% or higher cocoa content.
Melissa officinalis,
Salvia officinalis,
Yi-Gan San and BDW (Ba Wei Di Huang Wan),
Ginkgo biloba.
All five herbs are useful for cognitive impairment of AD. M. officinalis and Yi-Gan San are also useful in agitation, for they have sedative effects.
These herbs and formulations have demonstrated good therapeutic effectiveness but these results need to be compared with those of traditional drugs. Further large multicenter studies should be conducted in order to test the cost-effectiveness of these herbs for AD and the impact in the control of cognitive deterioration.
Literatuur
Akhondzadeh S, Noroozian M, Mohammadi M, Ohadinia S, Jamshidi AH. 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.
Akhondzadeh S, Noroozian M, Mohammadi M, Ohadinia S, Jamshidi AH, Khani M. Melissa officinalis extract in the treatment of patients with mild to moderate Alzheimer’s disease: a double blind, randomized and placebocontrolled trial. J Neurol Neurosurg Psychiatr 2003;74:863–6.
Iwasaki K, Satoh-Nakagawa T, Maruyama M, Monma Y, Nemoto M, Tomita N e cols. A randomized, observer-blind, controlled trial of the traditional Chinese medicine Yi-Gan San for improvement of behavioral and psychological symptoms and activities of daily living in dementia patients. J Clin Psychiatr 2005;66:248–52.
Iwasaki K, Kobayashi S, Chimura Y, Taguchi M, Inoue K, Cho S e cols. A randomized, double-blind, placebo-controlled clinical trial of the Chinese herbal medicine ‘Ba Wei Huang Wan’ in the treatment of dementia. J Am Geriatr Soc 1994;52:1518–21.
Birks J, Grimley EJ. Ginkgo biloba for cognitive impairment and dementia. The Cochrane Library, Issue 2, 2004. Oxford: Update Software.
Kennedy DO, Scholey AB, Tildesley NTJ, Perry EK, Wesnes KA. Modulation of mood and cognitive performance following acute administration of Melissa officinalis (lemon balm). Pharmacol Biochem Behav 2002;72:953–64.
Kennedy DO, WakeBallard C, O’Brien J, Reichelt K, Perry E. Aromatherapy as a safe and effective treatment for the management of agitation in severe dementia: the results of a double blind, placebo controlled trial. J Clin Psychiatr 2002;63:553–8.
Cerny A, Schmid K. Tolerability and efficacy of valerian/lemon balm in healthy volunteers: a double-blind, placebo-controlled, multicenter study. Phytoterapia 1999;70:221–8.
Wong AHC, Smith M, Boon HS. Herbal remedies in psychiatric practice. Arch Gen Psychiatr 1998;55:1033–44. 24. Carnat AP, Carnat A, Fraisse D, Lamaison JL. The aromatic and polyphenolic composition of lemon balm (Melissa officinalis L. subsp. officinalis) tea. Pharm Acta Helv 1998;72:301–5.
Mulkens A, Stephanou E, Kapetenadis I. Heterosides a genines volatiles dans les feuilles de Melissa officinalis L. (lamiaceae). Pharm Acta Helv 1985;60:276–8.
Mantle D, Eddeb F, Pickering AT. Comparison of relative antioxidant activities of British medicinal plant species in vitro. J Ethnopharmacol 2000;72:47–51.
Hohmann J, Zupko I, Redei D, Csanyi M, Falkay G, Mathe I, et al. Protective effects of the aerial parts of Salvia officinalis, Melissa officinalis and Lavandula angustifolia and their constituents against enzyme-dependent and enzyme independent lipid peroxidation. Planta Med 1999;65:576–8.
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;69:105–114.
Hirokawa S, Nose M, Amagaya S, Oyama T, Ogihara Y. Protective effect of hachimi-jio-gan, an oriental herbal medicinal mixture, against cerebral anoxia. J Ethnopharmacol 1993;40:201–6.
Hirokawa S, Nose M, Ishige A, Amagaya S, Oyama T, Ogihara Y. Effect of Hachimi-jio-gan on scopolamine-induced memory impairment and on acetylcholine content in rat brain. J Ethnopharmacol 1996;50:77–84.
Gagnier JJ, Boon H, Rochon P, Moher D, Barnes J, Bombardier C. CONSORT Group. Reporting randomized, controlled trials of herbal interventions: an elaborated CONSORT statement. Ann Intern Med 2006;144:364–7.
Referenties
Leopoldo Luiz dos Santos-Neto et al. | The Use of Herbal Medicine in Alzheimer's Disease. A Systematic Review. | eCAM | 2006: 3(4)441-445.
Top on the list, of course, is curcumin. Others include:
Coconut Oil: This remarkable substance contains approximately 66% medium chain triglycerides by weight, and is capable of improving symptoms of cognitive decline in those suffering from dementia by increasing brain-boosing ketone bodies, and perhaps more remarkably,within only one dose, and within only two hours.[23]
Cocoa: A 2009 study found that cocoa procyanidins may protect against lipid peroxidation associated with neuronal cell death in a manner relevant to Alzheimer's disease.[24]
Sage: A 2003 study found that sage extract has therapeutic value in patients with mild to moderate Alzheimer's disease.[25]
Folic acid: While most of the positive research on this B vitamin has been performed on the semi-synthetic version, which may have unintended, adverse health effects, the ideal source for this B vitamin is foliage, i.e. green leafy vegetables, as only foods provide folate. Also, the entire B group of vitamins, especially including the homocysteine-modulating B6 and B12,[26] may have the most value in Alzheimer's disease prevention and treatment.
Resveratrol: this compound is mainly found in the Western diet in grapes, wine, peanuts and chocolate. There are 16 articles on our website indicating it has anti-Alzheimer's properties.[27]
Other potent natural therapies include:
Gingko biloba: is one of the few herbs proven to be at least as effective as the pharmaceutical drug Aricept in treating and improving symptoms of Alzheimer's disease.[28] [29]
Melissa offinalis: this herb, also known as Lemon Balm, has been found to have therapeutic effect in patients with mild to moderate Alzheimer's disease.[30]
Saffron: this herb compares favorably to the drug donepezil in the treatment of mild-to-moderate Alzheimer's disease.[31]
As always, the important thing to remember is that it is our diet and environmental exposures that largely determine our risk of accelerated brain aging and associated dementia. Prevention is an infinitely better strategy, especially considering many of the therapeutic items mentioned above can be used in foods as spices. Try incorporating small, high-quality culinary doses of spices like turmeric into your dietary pattern, remembering that 'adding it to taste,' in a way that is truly enjoyable, may be the ultimate standard for determining what a 'healthy dose' is for you.
Notes:
*This statement is not meant to be used to prevent, diagnosis, treat, or cure a disease; rather, it is a statement of fact: the research indexed on our database indicates it
**Our professional database users are empowered to employ the 'Advanced Database Options' listed on the top of the Turmeric research page and after clicking the function "Sort Quick Summaries by Title Alphabetically" under "Available Sorting Options" they can quickly retrieve an alphabetical list of all 613 diseases relevant to the Turmeric research, and then choosing the "Focus" articles selection to the right of the "Alzheimer's disease" heading to see only the 30 study abstracts relevant to the topic.
Resources
[1] Ron Brookmeyer, Elizabeth Johnson, Kathryn Ziegler-Graham, H Michael Arrighi. Forecasting the global burden of Alzheimer's disease. Alzheimers Dement. 2007 Jul ;3(3):186-91. PMID: 19595937
[2] Nozomi Hishikawa, Yoriko Takahashi, Yoshinobu Amakusa, Yuhei Tanno, Yoshitake Tuji, Hisayoshi Niwa, Nobuyuki Murakami, U K Krishna. Effects of turmeric on Alzheimer's disease with behavioral and psychological symptoms of dementia. Ayu. 2012 Oct ;33(4):499-504. PMID:23723666
[3] V Chandra, R Pandav, H H Dodge, J M Johnston, S H Belle, S T DeKosky, M Ganguli. Incidence of Alzheimer's disease in a rural community in India: the Indo-US study. Neurology. 2001 Sep 25 ;57(6):985-9. PMID: 11571321
[4] GreenMedInfo.com, Declaring Chemical Warfare Against Alzheimer's.
[5] GreenMedInfo.com, Turmeric's Neuroprotective Properties (114 study abstracts)
[6] Laura Zhang, Milan Fiala, John Cashman, James Sayre, Araceli Espinosa, Michelle Mahanian, Justin Zaghi, Vladimir Badmaev, Michael C Graves, George Bernard, Mark Rosenthal. Curcuminoids enhance amyloid-beta uptake by macrophages of Alzheimer's disease patients. J Alzheimers Dis. 2006 Sep;10(1):1-7. PMID: 16988474
[7] Ava Masoumi, Ben Goldenson, Senait Ghirmai, Hripsime Avagyan, Justin Zaghi, Ken Abel, Xueying Zheng, Araceli Espinosa-Jeffrey, Michelle Mahanian, Phillip T Liu, Martin Hewison, Matthew Mizwickie, John Cashman, Milan Fiala. 1alpha,25-dihydroxyvitamin D3 interacts with curcuminoids to stimulate amyloid-beta clearance by macrophages of Alzheimer's disease patients. J Alzheimers Dis. 2009 Jul;17(3):703-17. PMID: 19433889
[8] Hongying Liu, Zhong Li, Donghai Qiu, Qiong Gu, Qingfeng Lei, Li Mao. The inhibitory effects of different curcuminoids onβ-amyloid protein, β-amyloid precursor protein and β-site amyloid precursor protein cleaving enzyme 1 in swAPP HEK293 cells. Int Dent J. 1996 Feb;46(1):22-34. PMID: 20727383
[9] Shilpa Mishra, Mamata Mishra, Pankaj Seth, Shiv Kumar Sharma. Tetrahydrocurcumin confers protection against amyloidβ-induced toxicity. Neuroreport. 2010 Nov 24. Epub 2010 Nov 24. PMID: 21116204
[10] Xiao-Yan Qin, Yong Cheng, Long-Chuan Yu. Potential protection of curcumin against intracellular amyloid beta-induced toxicity in cultured rat prefrontal cortical neurons. Neurosci Lett. 2010 Aug 9;480(1):21-4. PMID: 20638958
[11] Hong-Mei Wang, Yan-Xin Zhao, Shi Zhang, Gui-Dong Liu, Wen-Yan Kang, Hui-Dong Tang, Jian-Qing Ding, Sheng-Di Chen. PPARgamma agonist curcumin reduces the amyloid-beta-stimulated inflammatory responses in primary astrocytes. J Alzheimers Dis. 2010;20(4):1189-99. PMID:20413894
[12] G P Lim, T Chu, F Yang, W Beech, S A Frautschy, G M Cole. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci. 2001 Nov 1;21(21):8370-7. PMID: 11606625
[13] Xiao-Yan Qin, Yong Cheng, Long-Chuan Yu. Potential protection of curcumin against intracellular amyloid beta-induced toxicity in cultured rat prefrontal cortical neurons. Neurosci Lett. 2010 Aug 9;480(1):21-4. PMID: 20638958
[14] D S Kim, S Y Park, J K Kim. Curcuminoids from Curcuma longa L. (Zingiberaceae) that protect PC12 rat pheochromocytoma and normal human umbilical vein endothelial cells from betaA(1-42) insult. Neurosci Lett. 2001 Apr 27;303(1):57-61. PMID: 11297823
[15] R Douglas Shytle, Paula C Bickford, Kavon Rezai-zadeh, L Hou, Jin Zeng, Jun Tan, Paul R Sanberg, Cyndy D Sanberg, Bill Roschek, Ryan C Fink, Randall S Alberte. Optimized turmeric extracts have potent anti-amyloidogenic effects. Curr Alzheimer Res. 2009 Dec;6(6):564-71. PMID: 19715544
[16] Fusheng Yang, Giselle P Lim, Aynun N Begum, Oliver J Ubeda, Mychica R Simmons, Surendra S Ambegaokar, Pingping P Chen, Rakez Kayed, Charles G Glabe, Sally A Frautschy, Gregory M Cole.Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. Neurochem Int. 2009 Mar-Apr;54(3-4):199-204. Epub 2008 Nov 30. PMID:15590663
[17] Can Zhang, Andrew Browne, Daniel Child, Rudolph E Tanzi. Curcumin decreases amyloid-beta peptide levels by attenuating the maturation of amyloid-beta precursor protein.Gastroenterology. 2006 Jan;130(1):120-6. PMID: 2062201
[18] Ranjit K Giri, Vikram Rajagopal, Vijay K Kalra. Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor.J Neurochem. 2004 Dec;91(5):1199-210. PMID: 15569263
[19] Touqeer Ahmed, Anwarul-Hassan Gilani, Narges Hosseinmardi, Saeed Semnanian, Syed Ather Enam, Yaghoub Fathollahi. Curcuminoids rescue long-term potentiation impaired by amyloid peptide in rat hippocampal slices. Synapse. 2010 Oct 20. Epub 2010 Oct 20. PMID: 20963814
[20] M Garcia-Alloza, L A Borrelli, A Rozkalne, B T Hyman, B J Bacskai. Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model. J Neurochem. 2007 Aug;102(4):1095-104. Epub 2007 Apr 30. PMID:17472706
[21] Larry Baum, Alex Ng. Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer's disease animal models. J Alzheimers Dis. 2004 Aug;6(4):367-77; discussion 443-9. PMID: 15345806
[22] Silvia Mandel, Tamar Amit, Orit Bar-Am, Moussa B H Youdim. Iron dysregulation in Alzheimer's disease: multimodal brain permeable iron chelating drugs, possessing neuroprotective-neurorescue and amyloid precursor protein-processing regulatory activities as therapeutic agents. Prog Neurobiol. 2007 Aug;82(6):348-60. Epub 2007 Jun 19. PMID: 17659826
[23] Mark A Reger, Samuel T Henderson, Cathy Hale, Brenna Cholerton, Laura D Baker, G S Watson, Karen Hyde, Darla Chapman, Suzanne Craft. Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging. 2004 Mar;25(3):311-4. PMID: 15123336
[24] Eun Sun Cho, Young Jin Jang, Nam Joo Kang, Mun Kyung Hwang, Yong Taek Kim, Ki Won Lee, Hyong Joo Lee. Cocoa procyanidins attenuate 4-hydroxynonenal-induced apoptosis of PC12 cells by directly inhibiting mitogen-activated protein kinase kinase 4 activity. Free Radic Biol Med. 2009 May 15;46(10):1319-27. Epub 2009 Feb 25. PMID: 19248828
[25] S Akhondzadeh, M Noroozian, M Mohammadi, S Ohadinia, A H Jamshidi, M Khani. 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 Feb;28(1):53-9. PMID: 12605619
[26] Celeste A de Jager, Abderrahim Oulhaj, Robin Jacoby, Helga Refsum, A David Smith. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. Int J Geriatr Psychiatry. 2011 Jul 21. Epub 2011 Jul 21. PMID: 21780182
[27] GreenMedInfo.com, Resveratrol's Anti-Alzheimer's properties
[28] S Yancheva, R Ihl, G Nikolova, P Panayotov, S Schlaefke, R Hoerr,. Ginkgo biloba extract EGb 761(R), donepezil or both combined in the treatment of Alzheimer's disease with neuropsychiatric features: a randomised, double-blind, exploratory trial. Aging Ment Health. 2009 Mar;13(2):183-90. PMID: 19347685
[29] M Mazza, A Capuano, P Bria, S Mazza. Ginkgo biloba and donepezil: a comparison in the treatment of Alzheimer's dementia in a randomized placebo-controlled double-blind study.Eur J Neurol. 2006 Sep;13(9):981-5. PMID: 16930364
[30] S Akhondzadeh, M Noroozian, M Mohammadi, S Ohadinia, A H Jamshidi, M Khani. Melissa officinalis extract in the treatment of patients with mild to moderate Alzheimer's disease: a double blind, randomised, placebo controlled trial. J Neurol Neurosurg Psychiatry. 2003 Jul;74(7):863-6. PMID: 12810768
[31] Shahin Akhondzadeh, Mehdi Shafiee Sabet, Mohammad Hossein Harirchian, Mansoreh Togha, Hamed Cheraghmakani, Soodeh Razeghi, Seyyed Shamssedin Hejazi, Mohammad Hossein Yousefi, Roozbeh Alimardani, Amirhossein Jamshidi, Shams-Ali Rezazadeh, Aboulghasem Yousefi, Farhad Zare, Atbin Moradi, Ardalan Vossoughi. A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer's disease.Psychopharmacology (Berl). 2010 Jan;207(4):637-43. Epub 2009 Oct 20. PMID: 19838862
AD, a progressive irreversible neurodegenerative disorder characterized by the loss of certain cognitive functions, behavioral disturbances, and daily living difficulties, is the most common form of dementia found among elderly individuals [1]. This disease currently affects 27 million people all over the world [2]. The prevalence rate for AD has become the third greatest threat to the elderly, only behind cardiovascular disease and cancer [3].
Although neither a consensus concerning the pathogenesis of AD nor a perfect therapy for its treatment is available, it is now well accepted that multiple factors, including apoptosis, oxidative stress, excitotoxicity, and the disturbance of energy metabolism homeostasis, contribute to the progression of AD [4]. Especially, the aggregation and accumulation of extracellular and intracellular Aβ play a critical role in the pathogenesis of AD and result in impaired synaptic plasticity and memory [5]. As a key rate-limiting enzyme, α-, β-, and γ-site amyloid precursor protein cleaving enzyme (α-, β-, and γ-secretase) initiates the formation of Aβ by producing the peptide from APP [6]. APP can be cleaved in two ways, with formation of non-toxic Aβ 17–42 by α- and γ-secretases and the generation of toxic Aβ 1–42 by β- and γ-secretases [7]. Therefore, inhibiting the activity of β-secretases is important for treating AD due to their role in the direct cleavage of the Aβ domain at the N-terminus in APP [8]. These changes are closely associated with tau phosphorylation and PI3K/Akt/GSK3βsignaling pathway along with MAPK signaling. The Akt-mediated control of GSK3β activity is involved in tau hyperphosphorylation [9]. Aβ generated by the cleavage of APP triggers immune responses and activates microglial cells that engulf Aβ filaments, with secretion of various pro-inflammatory factors [9], [10]. In addition, neuron-related apoptosis and oxidative stress lead to neuronal damage [11].
Numerous in vitro and in vivo models have been used for studying AD. Various types of cells were stimulated with neurodegenerative exposures such as to subtypes of Aβ and acrolein. Aβ deposition causes synaptic plasticity and memory impairment and has been detected in AD patients at early stage [12]. Acrolein is not only a marker of lipid peroxidation but also an inducer of oxidative stress and an effector of tissue damage [13]. With growing evidence of the implication of acrolein in AD, the development of strategies to reduce its toxic effect is of great importance [12].
Cognitive impairments in animal models are analyzed with behavioral tests, such as MWM task and Y-maze, RAWM, novel object recognition as well as cued and contextual fear-conditioning tests, which are known to be sensitive to hippocampal-dependent learning and memory deficits. Specifically, TgCRND8 mice expressing human APP695 with the Swedish (K670N/M671L) and Indiana (V717F) mutations under regulatory control of the PrP gene promoter (heterozygous with respect to the transgene) on a C57BL/6 F3 background are used to breed the colony of experimental animals [14], while transgenic mouse overexpressing of APP/Aβ (Tg mAPP) is a well-used mouse model of AD [15], [16].
Despite great effort to discover a remedy for AD, no currently available drug can stop or cure this neurodegenerative disorder, and current treatments offer only small symptomatic benefits. The most commonly prescribed drugs are cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine, and NMDA antagonists such as memantine. Though approved by the FDA, these drugs are not recommended by the NICE in England and Wales due to “limited and largely inconclusive” evidence concerning their efficacy [17]. Nootropic agents such as piracetam are commonly prescribed in Europe for the treatment of dementia, including dementia associated with AD, but there are insufficient evidences to verify the efficacy of such drugs [18].
Historically, a number of medicinal herbs have been used to treat neurodegenerative diseases and cognitive disorders in traditional European, Ayurvedic, and Oriental medicines. Medicinal herbs consist primarily of multiple compounds and may influence multiple mechanisms with multi-target functions. This review concerns five phytochemicals, berberine, curcumin, GRg1, puerarin, and silibinin, that have been recently and mostly investigated as alternative treatments for AD and will discuss the advances in our knowledge about these phytochemicals derived from medicinal herbs based on available literature facts collected from books and scientific papers by electronic search (PubMed, ScienceDirect, and Google Scholar) ([Fig. 1]).
Berberine, an isoquinoline alkaloid, is one of the major components of Cortex Phellodendri and Rhizoma Coptidis (Coptis chinensis, Franch.; Ranunculaceae). Berberine has been used in herbal medicine for liver disease, skin inflammation, diarrhea, and other disorders due to its anti-diarrheal, anti-microbial, and anti-inflammatory effects [8], [19], [20], [21]. Specifically, several studies have reported that berberine possesses multiple pharmacological effects that culminate in neuroprotective action against cerebral ischemia, psychological depression, schizophrenia, anxiety, and AD [22], [23]. Asai et al. reported that berberine reduces extracellular Aβ production and BACE activity without changes on release of LDH in H4 neuroglioma (APPNL-H4) cells [8]. The production of both Aβ and β-secretase are inhibited by berberine compared with the control in human embryonic kidney 293 (HEK293) cells. Berberine increased the expression level of p-ERK1/2, demonstrating that it may inhibit the production of Aβ via an activation of ERK1/2-induced BACE activity in HEK293 [24].
In another study, the effect of berberine on Aβ-induced neuroinflammation was examined in primary and BV2 microglial cells. Pretreatment with berberine reduces Aβ-induced IL-6 production and MCP-1 release, as well as expression of Cox-2 and inducible i-Nos. Subsequently, NF-κB and the phosphorylation of IκB-α, Akt, p38 kinase, and ERK1/2, but not JNK, stimulated by Aβ, are regulated following treatment with berberine [25]. Moreover, pretreatment with berberine reduced Aβ-stimulated activities of LDH and TNF-α with down-regulation of TNF receptor 1 in SK-N-SH neuroblastoma cells [26].
In APP transgenic mice, berberine treatment improved cognitive impairment as reflected in reductions in errors in the MWM task with respect to both conventional reference memory and memory retention (probe trial). Aβplaque immunostaining in TgCRND8 mice was associated with reductions in both the number and the area of coronal sections of the cortex and hippocampus following treatment with berberine. Moreover, consistent with the indication that berberine treatment reduces the accumulation of total Aβ peptides in the brain, a significant reduction was found in the degree of microgliosis by Iba-1 burden and astrocytosis by GFAP burden. The mechanisms underlying the benefits of berberine on cognitive function and Aβ neuropathology in TgCRND8 mice were expressed for CTF, APP, and tau phosphorylation. An inhibition of PI3K/Akt/GSK3β activities in the TgCRND8 mouse brain influenced CTF and p-APP levels and led to a blockage of Aβ accumulation [27] ([Table 1]).
Curcumin from Curcuma longa
Curcumin, a hydrophobic polyphenol, is isolated from the rhizome of the herb Curcuma longa L. (Zingiberaceae). It is one of the active components of turmeric involved in antioxidant, anti-inflammatory, metal chelators, anti-amyloid, anti-tau, and neuroprotective activities [13]. In addition, curcumin has been reported to bind to Aβ and prevent aggregation [28] and protect against cell death, as indicated by increased cell viability and decreased TUNEL-positive cells in rat primary neuron cells infected by adeno-5 virus packaged with iAβ 1–42. Curcumin treatment decreased ROS level and protected from intracellular Aβ toxicity [12]. It also inhibited the expression of ROS in acrolein-induced toxicity on SK-N-SH human neuroblastoma cell with increasing LDH release. Lipid peroxidation and oxidative stress by acrolein were protected by curcumin treatment. In addition, the expressions of γ-GCS synthetase and RNS levels, except GSH, were restored by treatment of curcumin. Other oxidative damage marker expressions, such as those of Nrf2, NF-κB, Sirt1, and Akt, were regulated under the presence of curcumin [13].
In other type of human neuroblastoma (SH-SY5Y cells), curcumin treatment decreased Aβ-induced tau phosphorylation at Thr231 and Ser396. In addition, it increased the expression of GSK3β and the phosphorylations of Akt at Thr308 and Ser473 sites and suppressed up-regulation of PTEN [29]. These results were supported by a previous report about the effect of curcumin on production of Aβ in pAPPswe-transfected SH-SY5Y cells. Xiong et al. reported that the production of Aβ 40 and Aβ 42 was decreased by treatment with curcumin [29]. Curcumin reduced the activation of PS1 in both mRNA and protein levels in APP-overexpressing cells. This change was accompanied with decreased GSK3β mRNA and protein levels [30].
Furthermore, curcumin has shown beneficial effects through hippocampal-dependent memory improvement. Treatment with curcumin improved the spontaneous alternation behavior as well as the recognition memory task in Aβ-infused rats. Concerning protection of cognitive impairment, a decrease in SYN levels was blocked and the phosphorylation of tau protein in rat hippocampus was decreased under the presence of curcumin. The production of TNF-α and IL-1β and activation of GFAP immunocontent levels were decreased in curcumin-treated hippocampus compared with non-treated samples. Additionally, BDNF concentration and the phosphorylation of Akt and GSK3β revealed an increase after curcumin treatment [31] ([Table 2]).
Ginsenoside Rg1 from Panax notoginseng
GRg1, a major active component of Panax notoginseng (Burk.) F. H. Chen (Araliaceae), is used to treat central nervous system dysfunctions, especially those involving cognitive abilities such as learning and memory [32]. The activity of β-secretase was inhibited in a concentration-dependent manner and a dose-dependent reversal of Aβ-induced decreased cell viability was observed following treatment with GRg1 in PC12 cells. GRg1 appeared to prevent oxidative damage through inhibition of LDH efflux, NO production, ROS induction, and lipid peroxidation. Additionally, treatment with GRg1 blocked this Aβ-induced calcium increase. To confirm the influence of GRg1 on apoptosis, caspase-3 activity was investigated by measuring the proteolytic cleavage of the fluorogenic substrate Ac-DEVD-AMC. The Aβ-induced increase in caspase-3 activity was inhibited by treatment with GRg1 [33].
In addition, Li et al. reported that GRg1 displayed anti-Aβ neurotoxicity via p38 pathway activation in SK-N-SH neuroblastoma cells induced by Aβ-stimulated THP-1 supernatant. Pretreatment with GRg1 markedly decreased LDH leakage, indicating that Aβ‐induced neuronal injury can be blocked by GRg1. Along with decreased tau phosphorylation, GRg1 treatment resulted in elevated IL-1β and decreased SYN, number of MAP-2 positive cells, and activation of p38 MAPK, which is associated with elevations of phosphorylated tau [34]. In terms of apoptosis, some reports also found that increased cytokine release, including IL-1β, IL-8, and TNF-α, was inhibited by GRg1 pretreatment in conjunction with an up-regulation of Bcl-2 and a down-regulation of Bax. This, in turn, resulted in an increase in the Bcl-2/Bax ratio as well as a reduction in the activation of caspase-3 [35].
In addition, GRg1-treated cortical neurons from C57BL/6 mouse fetuses with Aβ 1–42 inhibited the expression of Cyt c in cytosolic fraction, whereas Cyt c levels in mitochondrial fractions were increased. Marked decrease in caspase-3 activity and TUNEL-positive apoptotic neurons were shown in GRg1-treated groups [36]. In cortical neurons from embryonic rat fetus, GRg1 treatment protected Aβ 25–35-induced cell death. Bcl-2/Bax ratio was increased with reduced caspase-9 and − 3 activities by GRg1 treatment. Release Cyt c from mitochondria was blocked with GRg1 treatment [37]. Similarly, increased LDH release was suppressed against cytotoxicity of Aβ25–35 under the presence of GRg1. GRg1 reduced the numbers of apoptotic cells, as shown in decreased annexin V+/PI− fraction. The ratio of Bcl-2/Bax was up-regulated and activation of caspase-3 was down-regulated by GRg1 treatment [38].
In an animal study, Fang et al. demonstrated the neuroprotective effects of GRg1 in transgenic AD mice. ELISA and immunostaining with an Aβ antibody revealed that Aβ plaque loads were lower in the cerebral cortex and hippocampus of GRg1-treated mAPP mice than in vehicle-treated mice. This lower accumulation of Aβ in the cortices of GRg1-treated mice stemmed from the inhibition of γ-secretase activity and did not affect levels of AChE-positive neurites in the entorhinal cortex. Compared with vehicle-treated mAPP mice, GRg1-treated mice were shown to improve their performance in RAWM task [39] ([Table 3]).
Puerarin from the radix of Pueraria lobata
Previous research has demonstrated that puerarin (from Pueraria lobata (Willd.) Ohwi.; Fabaceae), which has been widely used in traditional medicine for thousands of years, exhibits anti-oxidant, anti-myocardial, anti-ischemic retinopathy, and anti-hyperglycemic effects [40], [41]. Zou et al. reported that puerarin have a protective effect against Aβ-induced neurotoxicity in rat hippocampal neurons via various mechanisms. Pretreatment with puerarin decreased Aβ-induced cell death in cultured rat hippocampal neurons by inhibiting GSK-3β via activation of Akt [42]. Furthermore, puerarin treatment resulted in an increase in GSH-Px and CAT activities and a decrease in the production of ROS [43].
In addition, treatment with puerarin prevented Aβ 25–35-induced apoptosis, as a result of decrease of TUNEL-positive cells and annexin V+/PI− fraction. Puerarin-treated cells inhibited the expression of caspase-3 with increased expression of Bcl-2 and decreased expression of Bax [44]. Similarly, Zhang et al. demonstrated that puerarin protected against cybrid viability loss in mitochondrial transgenic neuronal cells. Annexin V+/PI−fraction and intracellular ROS levels were attenuated by puerarin treatment. In addition, the expression of Bax, Bcl-2, phosphorylation of JNK and p38 were regulated by treatment of puerarin [45].
Another study found that puerarin treatment resulted in a significant enhancement of MWM task against Aβinjection. Treatment with puerarin decreased Aβ-induced cell death in rat hippocampus via activation of Akt. Furthermore, the phosphorylation of Bad was increased, while the production of caspase-9 was decreased in puerarin-treated group [46] ([Table 4]).
Silibinin from the herb milk thistle (Silybum marianum)
Silibinin is a flavonoid derived from the herb milk thistle (Silybum marianum (L.) Gaertn.; Asteraceae) and is known to have anti-oxidative and anti-inflammatory properties [47]. Various studies have indicated that silibinin confers protection against oxidative stress in hepatocytes by decreasing lipid peroxidation, a sensitive marker of oxidative lipids and scavenging of free radicals [48], [49]. Silibinin is protective against Aβ-induced oxidative stress in SH-SY5Y human neuroblastoma cells. The aggregation of Aβ was markedly inhibited following treatment with silibinin in ThT binding assay and TEM imaging assay. The presence of silibinin with Aβincreased cell viability, whereas its absence decreased it. Additionally, the level of H2O2 in Aβ-treated cells decreased following incubation with silibinin [50].
In animal experiments, silibinin ameliorates Aβ-induced short-term memory impairment as measured by a spontaneous alternation behavior task (Y-maze test) although no significant differences in the number of spontaneous locomotor activities were observed. Recognition memory in novel object recognition tests was improved by silibinin in Aβ-injected mice, while the amounts of time spent exploring objects in training and retention sessions did not differ. To further explore the effects of silibinin on Aβ-induced oxidative stress, levels of MDA and GSH were analyzed. Treatment with silibinin appeared to decrease MDA levels and increase GSH levels in the hippocampus [51]. The cued freezing response and contextual freezing response were attenuated in silibinin-treated animals, indicating an impairment in associative memory. However, silibinin did not change the level of response to electric foot shock (flinching, vocalization, and jumping) in either group. A significant increase in nitrotyrosine, TNF-α, and i-Nos levels in the hippocampus and amygdala were reduced following treatment with silibinin compared with distilled water [52] ([Table 5]).
The aggregation and accumulation of extracellular and intracellular Aβ induce impaired synaptic plasticity and memory [4]. Three proteases, such as α-, β-, and γ-secretases, cleave APP and generate the physiological peptide Aβ along with increased production of CTFs [53], [54], [55]. These soluble peptides spontaneously aggregate to form Aβ oligomers and fibrils that are subsequently deposited within the brain to form amyloid plaques [56]. The intracerebroventricular administration of Aβ peptide induces histological and biochemical changes, memory deficits, oxidative damage, and inflammatory responses [4], [5]. Based on our review, berberine, GRg1, and silibinin appear to block the formation of Aβ via an inhibition of β-secretase activity. In addition, GRg1 suppressed γ-secretase activity.
The PI3K/Akt/GSK3β signaling pathway is associated with various aspects of AD pathology. PI3K regulates the trafficking of intracellular APP-CTFs, whereas GSK modulates APP processing and thereby influences the production of Aβ in neurons. Inhibition of PI3K contributes to tau phosphorylation and impairment in spatial memory. Suppressing GSK3 activity, which is induced by phosphorylation at specific serine residues (Ser 9 and Ser21) by Akt, has been demonstrated to contribute to the accumulation of Aβ in APP mice and the hyperphosphorylation of tau protein [57], [58], [59], [60], [61], [62]. Berberine, curcumin, and puerarin regulated the PI3K/Akt/GSK3β signaling pathway. Berberine increased the phosphorylation of Akt and GSK3β, resulting in decreases of APP-CTFs levels. In vitro and in vivo data demonstrated that curcumin exhibits significant increases in the phosphorylation of Akt and GSK3β. Puerarin also upregulated the phosphorylation of GSK3β and Akt.
The activation of glial cells and the expression of inflammatory mediators in conjunction with the presence of neurotoxic free radicals lead to neuroinflammation. Activated microglial cells induced by Aβ are able to engulf filament Aβ; thus, the decrease in the Iba-1 burden correlates with a reduced plaque burden [63], [64], [65]. Release of proinflammatory cytokines, such as IL-6, IL-1β, and TNF-α, along with chemokines is responsible for the initiation and progression of inflammatory responses [66], [67], [68]. Several studies have shown that IL-6 induces the processing of APP and regulates Aβ production [69]. Microglia and macrophages are a major source of TNF-α although TNF-α is also expressed to a lesser extent by GFAP-positive astrocytes, and IL-1β is expressed by neurons and astrocytes in response to AD-like pathology [66], [67]. High level of MCP-1 promotes the migration and recruitment of inflammatory cells [70], [71]. Furthermore, Aβ-induced MCP-1 mRNA expression is associated with the activation of the PI3K/Akt signaling pathway [72]. Additionally, NF-κB, and its key inhibitor, IκB-α, primary regulator of inflammatory processes in almost all cell types including neurons, are expressed in microglial cells that express i-Nos and Cox-2 [73], [74]. Previous studies have shown that the MAPK signaling pathways play an important role in the regulation of chemokine and pro-inflammatory cytokine production in microglia [75], [76]. Berberine, curcumin, and GRg1 suppressed the activation of microglial cells and neuroinflammation by blocking the production of proinflammatory cytokines. Berberine, GRg1, and puerarin inhibited NF-κB and MAPK signaling pathways. In particular, berberine decreased the Iba-1 burden, indicating a reduction in the degree of microgliosis. In addition, treatment with berberine reduced IL-6 production and MCP-1 release in microglial cells. and suppressed NF-κB translocation into the nucleus as well as the phosphorylation of IκB-α, ERK1/2, and p38. Curcumin treatment showed a significant decrease in activated microglia along with reductions in IL-1β and TNF-α. In case of GRg1, the content of IL-1β, IL-8, and TNF-α were reduced with the phosphorylation of p38. And puerarin attenuated the phosphorylation of JNK and p38, resulting in the protection against neuronal cell death.
Concerning neuron cell survival, the loss of neuron-related apoptosis is regulated by several intracellular signaling events [77]. During early apoptosis stages, the Bcl-2 protein family which includes anti-apoptotic molecules such as Bcl-2 and Bcl-xL and pro-apoptotic molecules such as Bax, Bak, Bid, and Bad, is related to the formation of channels in mitochondrial membranes. The Bcl-2/Bax ratio, in particular, is crucial for initiating apoptosis, and its translocation to the mitochondrial membrane may lead to the loss of mitochondrial membrane potential and increased mitochondrial permeability [78] which results in the release of Cyt c from mitochondria and the subsequent activation of procaspase-3 to caspase-3, eventually leading to apoptosis [79]. GRg1 and puerarin attenuated apoptosis by regulating anti-apoptotic and pro-apoptotic molecules. GRg1 regulated the ratio of Bcl-2/Bax, resulting in the release of Cyt c from mitochondria and the reduction of caspase-9 and caspase-3 activities. Puerarin protected cell death via up-regulating the ratio of Bcl-2/Bax and down-regulating the caspase-9 and − 3 activities which were induced by the phosphorylation of Bad.
Furthermore, it is well established that oxidative stress is involved in apoptosis in that excessive production of ROS can lead to neuronal apoptosis in AD [11], [80]. GSH and MDA are important intracellular anti-oxidants necessary for the formation of peroxynitrite and responsible for removing oxygen-free radicals [51], [81]. In addition, the activations of NF-κB, Sirt1, and Nrf2 pathways are related to protection of cells against oxidant damage as stress sensor molecules [82]. Curcumin, GRg1, puerarin, and silibinin exhibited protection against oxidative stress. Specifically, curcumin regulated γ-GCS expression and RNS level. And treatment with GRg1 inhibited the excessive generation of NO and MDA levels as well as ROS generation. Puerarin also decreased intracellular ROS generation while increasing GSH-Px and CAT activities in various neuronal cells. Silibinin decreased the levels of MDA, whereas GSH was increased in in vivo study.
Apart from the pathology, memory enhancement is one of major issues of AD. Loss of neuroblasts and markers, characteristic of striatal medium spiny neurons, belong to the process of neuronal cell death [83]. In terms of neurotrophic factors, BDNF promotes the survival of new hippocampal neurons [84]. Synaptic proteins take part in the development of nerve synapses and adjust their plasticity. SYN, one of the synaptic proteins, is a marker of synaptic distribution and synaptic density [85]. GRg1 increased SYN expression, and curcumin contributed to the formation of new neurons by regulating the synaptic proteins SYN and BDNF.
To date, evidence from recent studies suggests that commonly used medicinal herbs and their phytochemicals could potentially be used to treat AD. Although these studies focus on the efficacy of inhibiting AD development, and research on humans is limited, numerous findings demonstrate the possibilities of the use of medicinal herbs for the treatment of AD. The approach to investigate the potential treatment of AD may support drug development from herbal medicine.
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Les recherches sur les plantes avancent, mais la maladie ne recule pas. Bien au contraire. D’après l’INSERM, environ 900,000 personnes souffrent de la maladie aujourd’hui, et ce chiffre passera la barre des 1,3 million en 2020.
En tant qu’enfants, nous devons nous préparer à l’éventualité que cette maladie touche un jour l’un de nos parents. Et bien sur, pour nos vieux jours, nous devons nous préparer personnellement aussi.
De nombreuses plantes sont étudiées afin de trouver la nouvelle molécule miracle. Je ne vais pas toutes les passer en revues. Je vais par contre vous donner les 4 plus prometteuses. Quant à la première présentée ci-dessous, vous verrez que c’est un sujet un peu délicat. Il vaut mieux l’oublier.
Si vous prenez actuellement un traitement et que vous envisagez de prendre des plantes, vérifiez avec votre docteur ou pharmacien qu’il n’y ait pas d’interactions entre les deux.
Huperzia serrata
Maladie d'Alzheimer : Huperzia
Cette plante de la famille des lycopodes fait beaucoup parler d’elle. En effet, les chercheurs en ont tiré une substance appelée Huperzine A. Cette substance bloque l’action d’une enzyme, l’acetylcholinesterase.
Afin de comprendre à quoi cela peut nous servir, il faut remonter à l’une des premières hypothèses de la maladies d’Alzheimer, l’hypothèse dite “cholinergique”. Cette hypothèse postule que la maladie est causée par une synthèse réduite d’acetylcholine, un neurotransmetteur. Des médicaments ont donc été commercialisés, le donepezil et la galantamine par exemple, afin de bloquer la dégradation d’acetylcholine en inhibant l’action de l’enzyme qui la détruit.
L’huperzine A a donc exactement la même action que le donepezil.
Faisons une pause. Bien que l’huperzine A soit vendue comme complément alimentaire dans certains pays (les Etats-Unis par exemple), nous avons ici affaire à une molécule médicament. Pas une plante. Pas une grande variété de constituant qui agissent en synergie et d’une manière douce.
A utiliser un inhibiteur de l’acetylcholinesterase, autant se faire prescrire le médicament, avec l’accompagnement du docteur ainsi que des doses contrôlées et bien établies. Bref, elle n’a pas sa place dans l’escarcelle de l’herbaliste.
Le ginseng (Panax ginseng)
Maladie d'Alzheimer : ginseng
Voici une plante bien ancienne qui peut résoudre des déséquilibres qui sont définitivement bien modernes. Sa puissance ne cesse de m’étonner.
Tout d’abord, elle améliore nos facultés cognitives. Une étude réalisée sur des individus en bonne santé démontre que 400 mg par jour pendant 7 jours améliore la mémoire pendant une période de 1 à 6 heures après la prise(1). D’après cette étude, des doses de 200 ou 600 mg ne sont pas aussi efficaces.
Une étude réalisée cette fois sur des patients souffrant de la maladie d’Alzheimer démontre qu’une dose beaucoup plus élevée, 4,5 g tous les jours pendant une période de 12 semaines, améliore les performances cognitives d’une manière graduelle au cours de cette période(2). Lorsque la prise est stoppée, les performances retombent au niveau de celles du groupe placebo.
Le ginseng n’est pas fait pour tout le monde. En médecine chinoise, on l’utilise chez la personne en état de grande faiblesse et surtout chez la personne âgée, ce qui est une combinaison relativement courante chez la personne souffrant d’Alzheimer. Il peut parfois créer des états de surexcitation ou des explosions de colère.
Le ginseng se prend tous les matins pendant des périodes de plusieurs semaines. Commencez par de faibles doses de racine pulvérisée, entre 500 mg et 1 g par jour afin de voir si la personne tolère bien la plante. Au bout de deux semaines, vous pouvez augmenter à 3 g à 4 g. Vous pouvez fabriquer vos propres gélules à partir de la poudre (plus économique).
Le ginkgo biloba
Maladie d'Alzheimer : ginkgo
Qu’en est-il de l’arbre aux milles écus ?
Une étude démontre qu’une dose journalière de 120 mg à 240 mg pendant 26 semaines améliore d’une manière significative les performances cognitives chez les individus souffrant de maladie d’Alzheimer et de troubles neuropsychiatriques (dépression, apathie, hyperactivité, etc)(3).
Ceci est confirmé par une revue de 6 études cliniques qui conclue que le ginkgo améliore la cognition chez la personne souffrant d’Alzheimer sans effet secondaires ou indésirables(4).
Cet effet pourrait être du à une inhibition de la formation des plaques amyloïdes entre les neurones qui caractérise la maladie(5).
De plus, le ginkgo contient de puissants antioxydants qui protègent le cerveau contre les effets néfastes du stress oxydatif. Le stress oxydatif est fortement impliqué dans le développement de la maladie(6).
Utilisez un extrait standardisé à 24 % de ginkgolides et à 6 % de lactones terpéniques. Les doses sont de 120 mg à 240 mg par jour.
Le curcuma
Curcuma 9-5-1
De nombreuses études montrent que le curcuma pourrait être une thérapie efficace pour inhiber la formation des plaques amyloïdes et diminuer l’inflammation cérébrale chez la personne souffrant de maladie d’Alzheimer. Une étude en particulier mentionne une dose journalière de 1 à 4 g(7).
De nombreux facteurs sont impliqués dans le développement de la maladie : stress oxydatif, inflammation et développement de plaques amyloïdes.
Le curcuma, avec son action à large spectre, peut intervenir sur tous ces facteurs afin de ralentir la progression de la maladie :
Diminution de la formation des plaques amyloïdes
Ralentissement de la dégradation des neurones
Effet anti-inflammatoire et antioxydant
Ces trois points majeurs amènent une amélioration progressive des capacités à mémoriser(8).
Le curcuma est-il une panacée ? Bien sur que non, les choses ne sont jamais aussi simple. Mais il n’est pas bien coûteux et constitue aujourd’hui l’une des meilleures plantes pour freiner la progression de la maladie.
Le bacopa
Maladie d'Alzheimer : bacopa
Le bacopa (Bacopa monnieri) a une longue tradition d’utilisation en médecine ayurvédique. C’est l’une des plantes les plus intéressantes pour la gestion de la maladie d’Alzheimer(9). Les études sur les effets positifs du bacopa pour les problèmes de mémoire et de cognition sont encore dans leurs balbutiements(10).
C’est pour cela qu’il faut parfois laisser de coté les études cliniques et faire confiance à la tradition herbaliste. Le brahmi (son nom en médecine ayurvédique) a une longue histoire de régulation des troubles nerveux. Il régénère la personne et lui redonne ses capacités intellectuelles. Il améliore la mémoire, la concentration et la capacité à apprendre. Bref, un profil parfait pour contrer la maladie d’Alzheimer.
La plante se prend sous forme de teinture à raison de 60 gouttes 2 fois par jour dans un peu d’eau. Des doses plus élevées peuvent être utilisées selon le besoin. Les gélules sont parfois de piètre qualité.
Références
(1) Kennedy DO, et al. “Dose Dependent Changes in Cognitive Performance and Mood Following Acute Administration of Ginseng to Healthy Young Volunteers.” Nutr Neurosci. 4.4 (2001): 295-310.
(2) Lee ST, et al. “Panax ginseng Enhances Cognitive Performance in Alzheimer Disease.” Alzheimer Dis Assoc Disord. 22.3 (2008): 222-6.
(3) Schneider LS, et al. “A Randomized, Double-Blind, Placebo-Controlled Trial of Two Doses of Ginkgo biloba Extract in Dementia of the Alzheimer’s Type.” Curr Alzheimer Res. 2.5 (2005): 541-51.
(4) Janssen IM, et al. “Ginkgo biloba in Alzheimer’s Disease: A Systematic Review.” Wien Med Wochenschr. 160.21-22 (2010): 539-46.
(5) Yao ZX, et al. “Ginkgo biloba Extract (Egb 761) Inhibits Beta-Amyloid Production by Lowering Free Cholesterol Levels.” J Nutr Biochem. 15.12 (2004): 749-56.
(6) Perry G, Cash AD, Smith MA. Alzheimer Disease and Oxidative Stress. J Biomed Biotechnol. 2002;2(3):120-123.
(7) Baum L, Lam CW, Cheung SK, et al. Six-Month Randomized, Placebo-Controlled, Double-Blind, Pilot Clinical Trial of Curcumin in Patients with Alzheimer Disease. [In eng] J Clin Psychopharmacol. 2008 Feb; 28(1): 110-3.
(8) Mishra S, et al. “The Effect of Curcumin (Turmeric) on Alzheimer’s Disease: An Overview.” Ann Indian Acad Neurol. 11.1 (2008): 13-9.
(9) Apetz N, Munch G, Govindaraghavan S, Gyengesi E. Natural compounds and plant extracts as therapeutics against chronic inflammation in Alzheimer’s disease – a translational perspective. CNS Neurol Disord Drug Targets. 2014;13(7):1175-91.
(10) Pase MP, Kean J, Sarris J, Neale C, Scholey AB, Stough C. The cognitive-enhancing effects of Bacopa monnieri: a systematic review of randomized, controlled human clinical trials. J Altern Complement Med. 2012 Jul;18(7):647-52.
Texte Christophe Bernard