Alzheimer’s disease: Herbs & Supplements that Help

Dr. James Manos (MD)
July 5, 2019

Alzheimer’s disease (AD) prevention and treatment with herbs and dietary supplements 

The most popular studied herbs/ dietary supplements that have been studied for Alzheimer’s disease (AD)

Huperzine A

Animal and in vitro experiments have been conducted, and the mechanism of action for huperzine appears to be a combination of anticholinesterase activity and anti-glutamate, antioxidant, and neuroprotective effects. Huperzine A crosses the blood-brain barrier more effectively than the acetylcholinesterase inhibitors (AChEI) tacrine or donepezil and acts with greater potency than the acetylcholinesterase inhibitors (AChEI) tacrine, physostigmine, or galanthamine. Based on limited data, some beneficial effects are attributed to huperzine A in Alzheimer's disease, including increased general cognitive function, global clinical status, behavioral disturbances, and physical performance.

A meta-analysis showed that oral (by mouth) administration of huperzine A for 8 – 24 weeks (300 – 500 micrograms daily) led to significant improvements in mini-mental state examination (MMSE) and activities of daily living (ADL) – the results of meta-regression showed that the estimated effect size of MMSE and ADL was increased over the treatment time; in conclusion, huperzine A is a well-tolerated drug that could significantly improve cognitive performance and activities of daily living (ADL) in patients with Alzheimer's disease (AD).

The results obtained from a study using a sample of 3xTg-AD mice strongly suggest that the treatment with the two acetylcholinesterase inhibitors (AChEIs), huprine X (a new AChEI), and the structurally related huperzine A, not only improves the cognitive performance of the animals but also induces some neurochemical changes that could contribute to the beneficial effects observed.

A study in rats concluded that huperzine A had high bioavailability and more selective inhibition of AChE activity in the cortex and hippocampus – huperzine A fits more closely with the established criteria for ideal acetylcholinesterase (AChE) inhibitor to be used in clinical studies.

Hup A (huperzine A), a novel alkaloid isolated from the Chinese herb Huperzia serrata, is a potent and selective inhibitor of acetylcholinesterase (AChE), with rapid absorption and penetration into the brain in experimental animals. The inhibition is reversible with a longer duration of action. Hup A exhibited memory-enhancing activities in a broad range of the animal cognitive model. Compared to the classical drugs used in Alzheimer’s Phy, Tac (tacrine), and Gal (galantamine), Hup A has better therapeutic indices, and peripheral cholinergic side effects are minimal at therapeutic doses. These findings suggest that Hup A is a promising candidate for clinical development as a symptomatic treatment for Alzheimer’s disease (AD).

An in vitro study concluded that there is evidence that huperzine A protects neurons against amyloid β-peptide fragment 25 – 35 (Aβ25 – 35)-induced apoptosis (programmed cell death) via the inhibition of reactive oxygen species (ROS) formation and caspase-3 activity.

Α human study concluded that there is equal efficacy and safety between huperzine A in capsule and tablet for treating patients with Alzheimer’s disease (AD), and huperzine A (Hup) can reduce the pathological changes of the oxygen free radicals in the plasma and erythrocytes of patients with Alzheimer’s disease (AD).

A Cochrane review concluded that from the available evidence, Huperzine A seems to have some beneficial effects on the improvement of general cognitive function, global clinical status, behavioral disturbance, and functional performance, with no obvious serious adverse events for patients with AD. However, only one study was of adequate quality and size. There is, therefore, inadequate evidence to make any recommendation about its use.

The results of a study in patients with Alzheimer’s disease showed that about 58% (29/50) of patients treated with huperzine A showed improvements in their memory, cognitive, and behavioral functions; the efficacy of huperzine A was better than placebo (36%, 19/53) – the study concluded that huperzine A is a promising drug for symptomatic treatment of Alzheimer’s disease.

A study that evaluated the clinical efficacy and safety of huperzine Alpha in the treatment of patients with mild to moderate Alzheimer's disease (AD) showed that in comparison with the baseline data, there was an improvement of 4.6 points in cognition assessed by ADAS-Cog; an improvement of 2.7 points by MMSE (mini-mental state examination), an improvement of 1.5 points in behavior and mood by ADAS-non-Cog with 59.2% of the patients being on the mend clinically; and an improvement of 2.4 points by ADL with the capacity of ADL improved by at least 10% among 32.75% of the patients. Seventy percent of the patients in the huperzine Alpha group scored 1, approximately 3 points, and 27.8% scored 1, approximately two points by CIBIC-plus. In conclusion, a safe and effective medicine, huperzine Alpha remarkably improves the cognition, behavior, activity of daily life (ADL), and mood of Alzheimer's disease (AD) patients.

Turmeric/ curcumin

Various studies indicate a lower incidence and prevalence of Alzheimer’s Disease in India.

A human study found that those who occasionally ate curry (less than once a month) and often (more than once a month) performed better on a standard test (MMSE) of cognitive function than those who ate curry never or rarely.

Studies in animal models of Alzheimer's disease (AD) indicate a direct effect of curcumin in decreasing the amyloid pathology of Alzheimer's disease (AD).

The results of a study on rats suggest that curcumin improves spatial memory disorders (such disorders being symptomatic of Alzheimer's disease (AD)) in Aβ (1-40)-induced rats by downregulating GFAP expression and suppressing astrocytes (AS) activity.

In a preclinical study, curcumin-conjugated nanoliposomes were investigated as possible diagnostics and targeted drug delivery systems in Alzheimer’s disease, demonstrating strong labeling of Aβ deposits both in human tissue and in mice and in vitro downregulation of amyloid peptide secretion and prevention of Aβ-induced toxicity; in conclusion, curcumin-conjugated nanoliposomes could find application in the diagnosis and targeted drug delivery in Alzheimer’s disease (AD).

A study demonstrated that the levels of beta-amyloid in Alzheimer's disease mice that were given low doses of curcumin decreased by around 40% compared to those not treated with curcumin.

Recent reports have suggested curcumin's therapeutic potential in AD pathophysiology. In in vitro studies, curcumin has been reported to inhibit amyloid-β-protein (Aβ) aggregation, Aβ-induced inflammation, and the activities of beta-secretase and acetylcholinesterase. In in vivo studies, oral administration of curcumin has inhibited Aβ deposition, Aβ oligomerization, and tau phosphorylation in the brains of AD animal models and improved behavioral impairment in animal models.

The levels of beta-amyloid in Alzheimer's disease (AD) mice that were given low doses of curcumin were decreased by around 40% in comparison to those that were not treated with curcumin; also, low doses of curcumin also caused a 43% decrease in the so-called ΄΄plaque burden΄΄ in the brains of AD mice.

Several studies investigating the functionality of curcumin have shown that it not only inhibits amyloid sedimentation but also accelerates the disaggregation of amyloid plaque.

The results of a study in rats suggest that curcumin improves spatial memory disorders (such disorders being symptomatic of Alzheimer’s Disease (AD)) in Aβ(1-40)-induced rats by downregulating glial fibrillary acidic protein (GFAP) expression and suppressing astrocytes (AS) activity.

A study concluded that curcumin-conjugated nanoliposomes could be applied to diagnose and target drug delivery in Alzheimer’s disease (AD).

In another study, they synthesized water-soluble PLGA-coated- curcumin nanoparticles and coupled the nanoparticle with Tet-1 peptide, which has an affinity to neurons and possesses retrograde transportation properties; the results suggest that curcumin encapsulated-PLGA nanoparticles are able to destroy amyloid aggregates, exhibit anti-oxidative property and are non-cytotoxic (toxic for the cells); thus the PLGA-curcumin nanoparticles can be used as a drug with multiple functions in treating Alzheimer's disease proving it to be a potential therapeutic tool against this dreaded disease.

Acetylcarnitine (acetyl – L – carnitine, ALC, or ALCAR)

A recent meta-analysis of 21 double-blind clinical trials of ALC in treating mild cognitive impairment and mild Alzheimer’s disease showed significant efficacy vs. placebo.

Bacopa monnieri (Brahmi)

The results of a study in rats suggest the therapeutic potential of Bacopa monnieri (BM) in the treatment of Alzheimer's disease (AD) associated with cognitive decline.

Another study on rats showed that Bacopa monnieri extract improved the escape latency time in the Morris water maze test. The reduction of neurons and cholinergic neuron densities were also mitigated; these findings suggest that Bacopa monnieri is a potential cognitive enhancer and neuroprotectant against Alzheimer’s disease.

Idebenone (a synthetic product like coenzyme Q-10)

Idebenone is a new cerebro-active drug, effective in dementia disorders, particularly indicated in primary degenerative dementias, i.e. Alzheimer’s disease.

A study's results demonstrated that idebenone treatment was effective on memory, attention, and orientation and in slowing down the natural progressive worsening of Alzheimer’s disease.

Another study showed that patients randomized to idebenone showed a higher benefit from treatment than patients randomized to tacrine.

Citicoline (CDP – Choline/ INN)

Citicoline supplementation has been used to ameliorate memory disturbances in older people and those with Alzheimer's disease and has been proven to stimulate acetylcholinesterase (AChE) activity.

In patients with senile dementia, Alzheimer’s type citicoline stops the course of the disease, and neuroendocrine, neuroimmunomodulation, and neurophysiological benefits have been reported.

SAMe

A study concluded that Alzheimer’s disease (AD) is associated with lower cerebrospinal fluid (CSF) SAM levels. This is partly due to an association of the APOE4 allele with reduced SAM levels in the CSF.

AD is accompanied by reduced GST activity, diminished SAM, and increased S-adenosylhomocysteine (SAH), the downstream metabolic product resulting from SAM-mediated transmethylation reactions, when deprived of folate - thus, these findings underscore the critical role of SAM in the maintenance of neuronal health, suggesting a possible role of SAM as a neuroprotective dietary supplement for AD patients.

Vinpocetine

In three studies of older adults with memory problems associated with poor brain circulation or dementia-related disease, vinpocetine produced significantly more improvement than placebo on global cognitive tests reflecting attention, concentration, and memory.

A study in rats showed that treatment with vinpocetine for 21 days following the first i.c.v. Streptozotocin infusion significantly improved learning and memory in Morris water maze and passive avoidance paradigms. Also, vinpocetine significantly reduced oxidative-nitrosative stress, and chronic treatment with vinpocetine also significantly reduced the increase in acetylcholinesterase activity and lactate dehydrogenase levels.

Ginkgo Biloba

Ginkgo is widely used in Europe for treating dementia. It may protect nerve cells that are damaged in Alzheimer's disease. Several studies have found that ginkgo positively affects memory and thinking in people with Alzheimer's or vascular dementia. Studies suggest that ginkgo may help people with Alzheimer's: improve thinking, learning, and memory (cognitive function), have an easier time doing day-to-day activities, improve social behavior, and have fewer feelings of depression.

Several studies have found that ginkgo may work as well as some prescription Alzheimer's medications to delay the symptoms of dementia. However, other studies have failed to demonstrate the effectiveness of Ginkgo. There is no proof that taking ginkgo will help protect against dementia.

Some evidence shows that taking ginkgo leaf extract by mouth modestly improves symptoms of Alzheimer’s, vascular, or mixed dementia. However, there are concerns that many early ginkgo studies' findings may not be reliable. Although most clinical trials show ginkgo helps people with symptoms of Alzheimer’s disease and other dementias, some conflicting findings suggest it may be hard to determine which people might benefit.

A human study concluded that there is no evidence of relevant differences in the efficacy of the Ginkgo biloba special extract EGb 761 and the cholinesterase inhibitor donepezil in the treatment of mild to moderate Alzheimer’s dementia, so the use of both substances can be justified; in addition, the study contributed to the establishment of the efficacy and tolerability of the Ginkgo biloba special extract E.S. in the dementia of the Alzheimer type with special respect to moderately severe stages.

Phosphatidylcholine

A study concluded that the administration of egg phosphatidylcholine to mice with dementia increases brain acetylcholine concentration and improves memory.

Another study suggested that dietary supplementation of egg yolk phosphatidylcholine (PCh) improves the memory of Dull mice, particularly when given from gestation, and that the 2% PCh diet elicits a better response than the 8% PCh diet.

Another study concluded that the lower lysophosphatidylcholine/phosphatidylcholine (lyso-PC/PC) ratio in cerebrospinal fluid (CSF) of patients with Alzheimer’s disease (AD) may reflect alterations in the metabolism of choline-containing phospholipids in the brain in AD and suggests that PC species containing linoleic acid or arachidonic acid are equally involved.

Phosphatidylserine

The results of a study suggest that phosphatidylserine may be a promising candidate for treating memory loss in later life. Another study concluded that Soybean-derived phosphatidylserine is considered a safe food ingredient, and 6 months of Soy-PS supplementation could improve the memory functions of the elderly with memory complaints. A study showed that continuous oral administration of SB-tPS to aged male rats significantly improved performance in the water maze escape test similar to bovine brain cortex-derived phosphatidylserine, which restores cognitive function in patients with senile dementia).

Lecithin

A study concluded that the effects of lecithin are complex but that there may be a ΄΄therapeutic window΄΄ for the effects of lecithin in the condition and that this may be more evident in older patients.

Another study concluded that lecithin has a small additional benefit independent of tacrine.

L-Carnosine

The endogenous peptide carnosine may be potentially beneficial in treating Alzheimer’s disease because of its free-radical scavenger and metal-chelating properties.

A study that explored the effect of L-carnosine supplementation in the 3xTg-Alzheimer’s disease (AD) mouse showed that carnosine supplementation in 3xTg-AD mice promotes a strong reduction in the hippocampal intraneuronal accumulation of Aβ and complete rescues AD and aging-related mitochondrial dysfunctions – the study concluded that carnosine can be part of a combined therapeutic approach for the treatment of Alzheimer’s disease (AD).

Homotaurine (3 – APS)

Homotaurine, a small amino sulfonate compound that is present in distinct species of marine red algae, has been shown, in both in vitro and in vivo models, to provide a relevant neuroprotective (protective for the nerves) effect by its specific anti-amyloid activity and by its γ-aminobutyric acid type A receptor affinity.

A human study concluded that the primarily planned analyses did not show a significant treatment effect but were confounded by unexplained variance. Post-hoc analyses showed a significant treatment-related reduction in hippocampus volume (HV) loss. However, there was only a trend toward slowing decline on the Alzheimer Disease Assessment Scale cognitive subscale (ADAS-cog) and no slowing of decline on the Clinical Dementia Rating - Sum of Boxes (CDR-SB) assessment.

The findings of the analysis revealed statistically significant differences or statistical trends in favor of tramiprosate (homotaurine) on six ADAS-cog subscales, namely Following Commands, Language Comprehension, Ideational Praxis, Object Naming, Remembering Test Instructions, and Spoken Language Ability; this exploratory analysis suggests that tramiprosate (homotaurine) may have some benefit on memory, language, and praxis skills in mild to moderate Alzheimer’s disease (AD) individuals.

A new multi-center, double-blind, randomized, placebo-controlled study in a subset of the 1 052 patients of the A phase study describes the vMRI, cognitive and clinical results obtained in this subgroup; the exploratory analysis of the vMRI subgroup suggests that tramiprosate slows hippocampal atrophy, and reveals some evidence of a beneficial effect on cognition.

The results of a study indicate that 3-APS favors tau aggregation in tau-transfected non-neuronal cells and in neuronal cells; it was also demonstrated that 3-APS does not affect the binding of tau to microtubules but may prevent the formation of tau-actin.

Tramiprosate (3-amino-1-propanesulfonic acid; 3APS) was found to maintain Abeta in a non-fibrillar form, to decrease Abeta(42)-induced cell death in neuronal cell cultures, and to inhibit amyloid deposition. Treatment of TgCRND8 mice with Tramiprosate resulted in a significant reduction (approximately 30%) in the brain amyloid plaque load and a significant decrease in the cerebral levels of soluble and insoluble Abeta(40) and Abeta(42) (approximately 20 –30%). A dose-dependent reduction (up to 60%) of plasma Abeta levels was also observed, suggesting that Tramiprosate influences the central pool of Abeta, changing either its efflux or its metabolism in the brain.

Other herbs/ dietary supplements that have been studied for Alzheimer’s disease (AD)

(with bold black color are mentioned the herbs & dietary supplements that have been studied for their effectiveness; with bold green color are mentioned the herbs & dietary supplements that the author of this database considers more important than the rest– this is based on his personal point of view – based of course on their effectiveness on studies)


Black tea

The findings of a study suggest that theaflavins (TF1, TF2a, TF2b, and TF3), the main polyphenolic components found in fermented black tea, are potent inhibitors of amyloid-β (Aβ) and α-synuclein (αS) fibrillogenesis; thus, theaflavins might be used to remove toxic amyloid deposits.

Blueberries

A study on mice demonstrated that significant cognitive enhancement was observed in adult mice after short-term i.p. supplementation with the blueberry extract concentrated in polyphenols is closely related to higher brain antioxidant properties, and inhibition of AChE (acetylcholinesterase) activity – these findings stress the critical impact of wild blueberry bioactive components on brain function.

A study on mice showed that blueberry-fed (from 4 months of age) APP + PS1 transgenic mice showed no deficits in Y-maze performance (at 12 months of age) with no alterations in amyloid-beta burden.

The findings of a preliminary human study suggest that moderate-term blueberry supplementation can confer a neurocognitive benefit and establish a basis for more comprehensive human trials to study preventive potential and neuronal mechanisms.

Coenzyme Q-10

Coffee

Retrospective and prospective epidemiologic studies suggest that enhanced coffee/caffeine intake during aging reduces the risk of Alzheimer's disease (AD).

Studies in AD transgenic mice show that long-term caffeine administration protects against cognitive impairment and reduces brain amyloid-β levels/deposition through suppression of both β- and γ-secretase.

A study in mice that examined the effects of caffeinated and decaffeinated coffee on plasma cytokines, comparing their effects to caffeine alone, showed that in both AβPPsw+PS1 transgenic mice and non-transgenic littermates, acute i.p. treatment with caffeinated coffee greatly and specifically increased plasma levels of granulocyte-colony stimulating factor (GCSF), IL-10, and IL-6; the study concluded that coffee may be the best source of caffeine to protect against Alzheimer's disease (AD) because of a component in coffee that synergizes with caffeine to enhance plasma granulocyte-colony stimulating factor (GCSF) levels, resulting in multiple therapeutic actions against AD.

Aged garlic extract (AGE; also known as ‘Kyolic (TM)’)

The findings of an in vitro study suggest that consumption of garlic may lead to inhibition of Abeta aggregation in the human brain.

Panax ginseng

A human study concluded that Panax ginseng is clinically effective in the cognitive performance of Alzheimer's disease (AD) patients; the study showed that after the ginseng treatment, the cognitive subscale of ADAS and the MMSE score began to show improvements and continued up to 12 weeks.

Korean red ginseng (KRG; a form of Panax ginseng)

A human study concluded that Korean red ginseng (KRG) showed good efficacy for treating Alzheimer’s disease; however, further studies with larger samples of patients and a longer efficacy trial should be conducted to confirm the efficacy of KRG.

Green tea

In vitro studies have shown that green tea extract may protect neurons from Aβ amyloid-induced damage.

Omega – 3 fatty acids/ fish oil

A review concluded that a growing body of evidence from biological, observational, and epidemiological studies suggests a protective effect of omega 3 PUFA against dementia.

Another review concluded that the existing data favors a role for long-chain omega-3 fatty acids in slowing cognitive decline in elderly individuals without dementia but not for preventing or treating dementia, including Alzheimer’s disease.

Polyphenols/ red wine

Observations suggest that distinct polyphenolic compounds from red wines may be bioavailable at the organism level and beneficially modulate Alzheimer’s disease phenotypes through multiple Abeta-related mechanisms.

It has been previously found that treatment with Cabernet Sauvignon reduced the generation of AD-type amyloid-beta (Abeta) peptides.

A new study suggests that muscadine treatment attenuates Abeta neuropathology and Abeta-related cognitive deterioration in Tg2576 mice. These observations suggest that distinct polyphenolic compounds from red wines may be bioavailable at the organism level and beneficially modulate Alzheimer’s disease phenotypes through multiple Abeta-related mechanisms.

Saffron (dried stigmas of the plant Crocus sativus)

A study suggested that in the short term, saffron is safe and effective in mild to moderate Alzheimer’s disease.

Another study showed that saffron at this dose was effective, like donepezil, in treating mild-to-moderate AD after 22 weeks.

Another study demonstrated the effectiveness of crocin in antagonizing the cognitive deficits caused by intracerebroventricular streptozocin STZ in rats and its potential in treating neurodegenerative diseases such as Alzheimer's.

Aloe polymannose multi-nutrient complex (APMC) formula

The results of a study on patients with Alzheimer’s disease showed improvements in both clinical and physiological outcomes for a disease that otherwise has no standard ameliorative remedy.

Rosmarinic acid

An in vitro study concluded that although the mechanism by which curcumin and rosmarinic acid inhibit fAbeta formation from Abeta and destabilize preformed fAbeta in vitro remains unclear, they may be candidates as therapeutics for Alzheimer’s disease.

Beta-glucans

Bilberry & blackcurrant

The data from a study on mice suggests that anthocyanin-rich bilberry and blackcurrant diets favorably modulate amyloid precursor protein (APP) processing and alleviate behavioral abnormalities in a mouse model of Alzheimer's disease (AD).

Cinnamon

An in vitro study indicated that the ethanol extract of cinnamon may be a new potential resource of natural antioxidant and anticholinesterase compounds.

In a study, the authors identified a natural substance based on cinnamon extract (CEppt), which markedly inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ in neuronal PC12 cells – when administered to an AD fly model, CEppt rectified their reduced longevity, fully recovered their locomotion defects and totally abolished tetrameric species of Aβ in their brain; furthermore, oral administration of CEppt to an aggressive AD transgenic mice model led to a marked decrease in 56 kDa Aβ oligomers, reduction of plaques and improvement in cognitive behavior.

Cranberry

In laboratory tests, cranberry seems to protect somewhat against Alzheimer’s disease.

Fisetin & quercetin

Fisetin (3,3',4',7-tetrahydroxyflavone) is neuroprotective, induces neuronal differentiation, enhances memory, and inhibits the aggregation of the amyloid beta-protein (Abeta) that may cause progressive neuronal loss in Alzheimer's disease. A study investigated the structural requirements for the anti-amyloidogenic activity of fisetin by comparing the effects of several structurally related flavonoids on Abeta fibril formation in vitro. Among the ten flavonoids tested, fisetin, 3',4',7-trihydroxylflavone, 3,3',4'-trihydroxyflavone, luteolin, quercetin, and myricetin inhibited Abeta fibril formation. On the other hand, 3,3',7-trihydroxyflavone, 5-deoxykaempferol, chrysin, and kaempferol enhanced Abeta fibril formation. These results suggest that the 3',4'-dihydroxyl group, but not the 3- or 7-hydroxyl group, is essential for the inhibitory effect of fisetin on Abeta fibril formation.

Holy basil (Tulsi) extract

In a study, it increased step-down latency and acetylcholinesterase inhibition significantly.

Kale

A study mentions that kale seeds were the most effective Acetylcholinesterase (AChE) inhibitor.

kudzu

A study concluded that puerarin, an isoflavone purified from the Chinese herb radix of kudzu, may act as an intracellular reactive oxygen species (ROS) scavenger and protect neurons against oxidative stress-induced apoptosis (programmed cell death).

Lemon balm

A few studies have found that lemon balm may help improve cognitive function and decrease agitation in people with Alzheimer’s.

A study concluded that lemon balm extract is of value in the management of mild to moderate Alzheimer’s disease and has a positive effect on agitation in such patients.

Another study concluded that doses of lemon balm at or above the maximum employed here can improve cognitive performance and mood and may be a valuable adjunct in treating Alzheimer’s disease.

Another study on Alzheimer’s disease showed a sustained improvement in Accuracy of Attention following 600 mg of Melissa and time- and dose-specific reductions in both Secondary Memory and Working Memory factors. Self-rated ΄΄calmness΄΄, as assessed by Bond-Lader mood scales, was elevated at the earliest time points by the lowest dose, whilst ΄΄alertness΄΄ was significantly reduced at all time points following the highest dose.

Alpha-lipoic acid

A study suggests that treatment with alpha-lipoic acid might be a successful ΄΄neuroprotective΄΄ therapy option for Alzheimer’s disease.

Melatonin

It may be helpful in preventing and treating Alzheimer’s disease by inhibiting the aggregation of the beta-amyloid plaques that cause the death of the neurons and the formation of neurofibrillary tangles in this disease.

A review concluded that melatonin treatment may be effective for the treatment of dementia-related psychopathologic behavior disturbances. However, no evidence was found to support melatonin's effectiveness in treating cognitive impairment.

Milk thistle/ Silymarin

In vivo studies indicated a significant reduction in brain Aβ deposition and improved behavioral abnormalities.

Linoleic acid (an omega-6 fatty acid)

In a study, the authors found a previously unrecognized linoleic acid (an omega-6 fatty acid) deficiency in the early phase of neurodegeneration that was strongly supported by an increased compensatory mead acid (an omega-9 fatty acid) level; these findings suggest the importance of creating new dietary manipulation strategies to counteract disease progression.

Resveratrol

The findings of a study demonstrate a proteasome-dependent anti-amyloidogenic activity of resveratrol and suggest that this natural compound has therapeutic potential in Alzheimer’s disease.

Rhodiola rosea

A study demonstrated that Rhodiola rosea L. roots have potent antidepressant activity by inhibiting MAO-A and may also find application in the control of senile dementia by their inhibition of MAO-B.

Rosemary (carnosic acid) & lemon & levander & orange essential oils

A study examined the curative effects of aromatherapy in dementia in 28 elderly people, 17 of whom had Alzheimer’s disease, by using rosemary and lemon essential oils in the morning and lavender and orange in the evening – the study concluded that aromatherapy is efficacious non-pharmacological therapy for dementia and that aromatherapy may have some potential for improving cognitive function, especially in Alzheimer’s disease patients.

Eleuthero (called wrongly by some as Siberian ΄΄ginseng΄΄)

Extracts of Eleuthero (the rhizome of Eleutherococcus senticosus) were shown to have protective effects on the regeneration of neurites, and the reconstruction of synapses in rat cultured cortical neurons damaged by amyloid β (Aβ)(25-35) and eleutheroside B was one of the active constituents.

In an in vitro study, the ethyl acetate, n-butanol, and water fractions from the methanol extract of Eleuthero showed protective effects against Aβ-induced neuritic atrophy, and the compounds eleutheroside B, eleutheroside E and isofraxidin showed obvious protective effects against Aβ (25-35)-induced atrophies of axons and dendrites.

Chinese skullcap (Scutellaria baicalensis)

The results of a study indicated that Scutellaria baicalensis may possess therapeutic potential for the prevention of Alzheimer’s disease and vascular dementia.

Soybeans

A study in rats suggested that soy meal is a potential alternative to estrogen in preventing and treating Alzheimer’s disease.

Spirulina

A study in mice concluded that Spirulina platensis may prevent the loss of memory, possibly by lessening Aβ protein accumulation, reducing oxidative damage, and mainly augmenting the catalase activity.

Goji berry (Wolfberry)

A study showed that polysaccharides derived from wolfberry exerted neuroprotective effects on cortical neurons exposed to homocysteine. Therefore, LBA can potentially be a disease-modifying agent for the prevention of Alzheimer’s disease.

Yokukansan

An in vitro study demonstrated that yokukansan (YKS), a traditional Japanese medicine, inhibited amyloid-beta (β) protein (Aβ) aggregation in a concentration-dependent manner.

An in vivo study demonstrated that YKS and Uncaria hook (UH), a YKS constituent, prevented cerebral Aβ accumulation.

Another study indicated that Yokukansan, Senkyu (a component of Yokukansan), and ferulic acid (the content of the above two drugs) are protective against endoplasmic reticulum (ER) stress-induced neuronal cell death and may provide a possible new treatment for Alzheimer’s disease (AD).

Cat’s claw

Dark chocolate

Neurodegenerative disorders such as Alzheimer's disease (AD) are associated with oxidative stress. It has been suggested that apoptosis (programmed cell death) is a crucial pathway in neuronal cell death in AD patients. 4-Hydroxynonenal (HNE), one of the aldehydic products of membrane lipid peroxidation, is reported to be elevated in the brains of AD patients and mediates the induction of neuronal apoptosis in the presence of oxidative stress. The results of a study indicate that cocoa procyanidin fraction (CPF) and its major antioxidant procyanidin B2 protect rat pheochromocytoma PC12 cells against 4-Hydroxynonenal (HNE) –induced apoptosis (programmed cell death) by blocking MKK4 activity as well as ROS (reactive oxygen species) accumulation.

Devil’s claw

The result of an in vitro study that tested the ability of extracts, phenylethanoid-containing fractions, and the major phenylethanoid glycoside isolated from the Devil's claw cultures to inhibit acetylcholinesterase and butyrylcholinesterase and the antioxidant activity in iron-related systems indicated that the phenylethanoid fractions may be attractive for various commercial purposes since they displayed significant cholinesterase inhibitory activity (even higher than that of pure galantamine (a medicine used for Alzheimer’s disease) in the case of butyrylcholinesterase inhibition assay.

Almonds

A study that investigated the effect of Prunus amygdalus (PA) (almond) nuts on cognitive functions, total cholesterol levels, and cholinesterase (ChE) activity in scopolamine-induced amnesia in rats showed that PA at the above-mentioned doses after 7 and 14 days of administration in the respective groups significantly reversed scopolamine (1 mg/kg i.p.)-induced amnesia, as evidenced by a decrease in the transfer latency in the EPM task and step-down latency in the passive avoidance task. PA reduced brain ChE activity in rats. PA also exhibited remarkable cholesterol and triglyceride-lowering properties and a slight increase in glucose levels in the present study. In conclusion, because diminished cholinergic transmission and an increase in cholesterol levels appear responsible for the development of amyloid plaques and dementia in Alzheimer patients, Prunus amygdalus (PA) (almond) may prove to be a useful memory-restorative agent. It would be worthwhile to explore this plant's potential in managing Alzheimer's disease.

Apple

Gain-of-function mutations in the presenilin-1 (PS-1) promote Alzheimer's disease (AD) by increasing reactive oxygen species (ROS), at least part of which is derived from an accompanying increase in the generation of amyloid-beta (Abeta). A study on mice demonstrated that apple juice concentrate (AJC) contained levels of S-adenosylmethionine (SAM) comparable to those capable of suppressing presenilin-1 (PS-1) overexpression, suggesting that the SAM content of AJC represents a potential mechanism for preventing PS-1 overexpression, and further highlighting the possibility that AJC provides neuroprotection by mechanisms in addition to its antioxidant potential.

A study in mice demonstrated that apple juice concentrate (AJC), administered in drinking water, maintains acetylcholine levels that otherwise decline when adult and aged mice are maintained on the above deficient diet.

Thanks for reading!