Emerging research has explored some natural compounds for stopping Alzheimer’s disease in its tracks or slowing it down. However, there’s no strong evidence to support any of these complementary or alternative approaches. Read on for a full breakdown of lifestyle changes, supplements, dietary approaches that have been studied.
There is currently no known cure for Alzheimer’s disease (AD).
Alzheimer’s disease is a life-changing diagnosis that requires careful medical monitoring and treatment, as well as a safe and supportive environment.
Current Alzheimer’s medications help initially reduce symptoms of memory loss and other cognitive problems. Two classes of drugs are typically prescribed:
Doctors may add other medications to manage specific symptoms, such as low mood or behavioral changes.
If your goal is to improve your brain health to deal with your cognitive issues – including those of poor memory, forgetfulness, or personality changes – it’s important to talk to your doctor, especially your symptoms are significantly impacting your daily life.
Major memory and behavior changes – such as forgetting recent events or conversations, misplacing your possessions, getting lost in familiar places, having trouble finding the right words to describe something, and low mood or apathy – are all reasons to see a doctor.
Many conditions, some of which are treatable, can result in poor memory or other symptoms of cognitive impairment or dementia.
Your doctor should diagnose and treat the condition causing your symptoms.
Likewise, if you are concerned about the symptoms of someone close to you, talk to them about scheduling a doctor’s appointment and going there together.
Many people with cognitive decline are not fully aware of their own memory and behavior, and the support of loved ones can be indispensable.
Scientists are investigating whether any natural strategies can target Alzheimer’s disease, either attempting to stop or slow down the disease. Research is in the early stages and we’ve outlined it below for informational purposes.
According to the National Center for Complementary and Alternative Medicine (NCCIH) :
“Currently, there is no strong evidence that any complementary health approach or diet can prevent cognitive impairment.”
Remember, changes in brain chemistry are not something that people can change on their own with the approaches listed below. Instead, the factors listed here are meant to support overall brain health and well-being.
The main idea is that living a healthy lifestyle, eating nutritious foods, getting quality sleep, and engaging in exercise is critical for maintaining a healthy brain – and sharp memory – as we age [2, 3, 4, 5].
You may try the additional strategies listed below if you and your doctor determine that they could be appropriate.
Read through the approaches listed here and discuss them with your doctor before trying them out. None of these strategies should ever be done in place of what your doctor recommends or prescribes.
Have in mind that supplements have not been approved by the FDA for medical use. Supplements generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective.
Lastly, supplement-drug interactions can be dangerous and, in rare cases, even life-threatening. Many supplements may interact with Alzheimer’s disease medications. That’s why it’s so important to consult your doctor before supplementing and let them know about all drugs and supplements you are using or considering.
The following substances and lifestyle changes have shown promise for reducing Alzheimer’s disease symptoms in limited, low-quality clinical studies.
There is currently insufficient evidence to support the use of the approaches listed below in people with Alzheimer’s disease, and they should never replace what your doctor prescribes.
Review studies show that exercise may help patients with Alzheimer’s disease. Limited evidence suggests that it may improve cognitive function, boost mood, and potentially slow the rate of decline in the patient’s ability to take care of themselves [6, 7, 8, 9, 10, 11].
In a trial of 50 patients with mild Alzheimer’s disease (aged 50-80 years), aerobic exercise (cardio) improved cognitive function and quality of life after 3 months of training .
In another trial of 76 older people with probable Alzheimer’s, aerobic exercise improved memory and reduced shrinkage of the hippocampus after 26 weeks. The hippocampus is the brain’s main hub for memory and emotions, and it drastically and progressively shrinks in people with Alzheimer’s .
Patients with Alzheimer’s disease who took walks regularly had reduced symptoms of depression and found it easier to perform their daily activities, according to a small trial of 26 people. A physical training program also improved balance, mobility, and reduced the risk of falling in 40 patients with Alzheimer’s [13, 14].
Interestingly, researchers conducting rodent studies hypothesize that physical activity leads to a decreased rate of beta-amyloid formation in the brain, a major factor of Alzheimer’s disease. This hasn’t been proven in humans .
Despite overall encouraging clinical findings, large-scale, multi-center trials are needed to verify the effects of different types of exercise on cognitive function in people with Alzheimer’s.
Based on research in animals and cells, some scientists think that antioxidants such as vitamin E, turmeric, and saffron may have the potential to protect neurons against free radical damage, restore acetylcholine – the most important neurotransmitter for memory and learning levels – and prevent the formation of beta-amyloid deposits. However, no clinical evidence backs them up .
An observational study of ~5,400 people found an association between higher intakes of vitamin E with lower rates of dementia, including Alzheimer’s disease. However, this study dealt with associations only, which means that a cause-and-effect relationship wasn’t investigated .
In a trial of 613 patients with mild-to-moderate Alzheimer’s, vitamin E at a dose of 2,000 IU/d appeared to slow down disease progression and functional decline compared to memantine and placebo .
However, the results have been mixed. Neither vitamin E (2,000 IU/d) nor donepezil improved mild cognitive impairment (precursor state to dementia) in a trial of 769 people in the long term .
In another trial of ~3,800 men aged 60 years or over, a combination of vitamin E and selenium could not prevent the development of dementia any more than placebo. The dosage used was 400 IU vitamin E and 200 mcg selenium. The authors think that this study may have failed because the dose of vitamin E was too low .
All in all, However, more quality research is needed to determine the safety and effectiveness of 2,000 international units daily of Vitamin E in people with Alzheimer’s or dementia.
Moreover, a study of 54 patients suggested that saffron is as effective as donepezil (a cholinesterase inhibitor) at reducing the symptoms of mild-to-moderate Alzheimer’s disease. The side effects appeared to be similar between both treatments with the exception of vomiting, which occurred significantly more often in the donepezil group .
Large-scale studies are lacking and the existing research had several limitations. Further work is needed to determine the safety and effectiveness of saffron in this population.
Despite this, no valid scientific evidence supports its use in people with Alzheimer’s. Clinical studies have been mixed, possibly due to resveratrol’s poor bioavailability.
In a trial of 119 patients with mild-to-moderate Alzheimer’s disease, 500-2,000 mg resveratrol appeared to halt the formation of beta-amyloid deposits in the brain, a hallmark of the disease. However, patients’ symptoms were unchanged after 52 weeks .
Resveratrol, in combination with fish oil and vitamin D, improved cognitive function in a small trial with 18 patients with Alzheimer’s disease. However, only those patients who had the E3 variant of the ApoE gene experienced improvement; those with the ApoE4 variant did not. The dosage was relatively low, at 150 mg daily .
Interestingly, the authors suggested that patients who received resveratrol also had lower rates of cancer, though this remains unproven. They hypothesize that targeting SIRT1 might protect not only against Alzheimer’s, but also other age-related diseases. It’s impossible to draw such conclusions from the existing data, though .
Additionally, resveratrol protected the neurons of animals with Alzheimer’s disease and inhibited the formation of beta-amyloid deposits in mice. Scientists are exploring similar mechanisms in cell-based studies [25, 26, 27].
Besides activating SIRT1, certain research groups are exploring whether resveratrol might improve autophagy. Autophagy breaks down and recycles diseased and damaged cells. Limited evidence points to impaired autophagy in Alzheimer’s disease .
Alzheimer’s disease patients often experience poor sleep and disruptions of their sleep-wake cycle. Many suffer from “sundowning,” a worsening of mood and cognitive function in the late hours of the evening .
A study of 18 people suggested that melatonin receptors (MT1, MT2) are low in elderly patients with Alzheimer’s disease. When these receptors are low, melatonin cannot effectively do its job in the brain .
Slow-release melatonin improved sleep quality and cognitive function in a trial of 80 patients with mild-to-moderate Alzheimer’s disease at 2 mg/day .
In another trial of 14 Alzheimer’s disease patients, 9 mg of melatonin daily improved sleep and halted the decline in cognitive function normally seen in the disease .
Melatonin is also being researched in people with mild cognitive impairment, the precursor state to dementia. In a trial of 50 people with mild cognitive impairment, 3-9 mg of melatonin improved cognitive function, mood, and sleep quality .
In a trial of 189 patients with Alzheimer’s disease, bright light in the morning and melatonin at night improved their sleep and cognitive function. Another study of 50 patients found similar results [34, 35].
Using cell-based mediums, researchers are also investigating whether melatonin can prevent cell death caused by synthetic beta-amyloid proteins that are similar to those that trigger Alzheimer’s disease .
Huperzine A is sparking the interest of some scientists as a natural compound that shows promise for Alzheimer’s disease. This is mainly because of its ability to increase acetylcholine levels and improve memory in animals .
Huperzine A has been suggested to improve blood flow in the brain, reduce free radical damage, and protect against excess glutamate. Clinical trials in China have claimed it improves cognitive function and quality of life in Alzheimer’s disease patients .
In a systematic review of different interventions for Alzheimer’s, combined data from multiple studies was used to suggest that huperzine A may have a statistically significant effect in reducing cognitive decline during Alzheimer’s disease .
While the early results are promising, there are some major limitations to note. For one, the quality of these studies is relatively low. Many were poorly-controlled or they were not designed to rule out biases from the authors. In addition, most of the studies and clinical trials were from China, which raises some questions about their overall validity.
In a large trial of 210 patients with mild-to-moderate Alzheimer’s disease, 0.8 mg of Huperzine A daily improved cognitive function, while 0.4 mg did not .
Some smaller trials did find an effect at a dose of 0.4 mg. In a trial of 50 patients with AD, 0.4 mg of Huperzine A improved memory, cognitive function, and daily functioning. Another trial of 60 patients found similar results [41, 42].
By decreasing the inflammation triggered by beta-amyloid proteins, Huperzine A was hypothesized to stop cell death (apoptosis) in a cell-based study .
A review of observational studies revealed Alzheimer’s disease patients tend to have lower blood levels of vitamin D than healthy people. Another review study found that blood levels of vitamin D less than 50 nmol/L were associated with a higher risk of Alzheimer’s disease [45, 46].
A trial of 52 people revealed that vitamin D reduced beta-amyloid deposits and improved cognitive function, but only in those with mild cognitive impairment which precedes Alzheimer’s disease. Patients with early Alzheimer’s disease did not experience improvement .
In a study of 43 patients with Alzheimer’s disease, vitamin D in combination with memantine improved cognitive function. Interestingly, neither vitamin D nor memantine alone was effective in this experiment .
Scientists are also using cell studies to explore if vitamin D stimulates immune cells to break down beta-amyloid deposits in the brain. At the same time, vitamin D is hypothesized to protect healthy brain cells against damage from beta-amyloid proteins, but this remains clinically unverified [49, 50].
In another trial of 57 patients with Alzheimer’s disease, 300 mg/d phosphatidylserine improved cognitive function. In rat brains, it reduced oxidative damage by boosting the antioxidant superoxide dismutase (SOD) .
Normally, the brain uses sugar as its primary energy source. But one theory states that, in Alzheimer’s disease, the brain’s ability to use sugar for fuel is impaired. In a small trial of 8 people with probable Alzheimer’s, 500 mg/d phosphatidylserine improved the brain’s ability to use sugar for energy [53, 54].
Scientists are investigating whether phospholipids, including phosphatidylserine, inhibit inflammation and the formation of beta-amyloid proteins in cells .
In another small trial of 12 elderly people with cognitive dysfunction, 2 g/ green tea also improved cognitive function. Unfortunately, these results were not repeated in a larger trial with 33 people [58, 59].
Interestingly, an observational study of 1,000 elderly people in Japan suggested that those with the highest green tea consumption had the lowest rates of cognitive impairment .
A recent mouse study claimed that a combination of EGCG and ferulic acid seemed more effective at treating Alzheimer’s disease than either compound alone. This combination reduced cognitive impairments in the mice .
Further clinical trials are needed.
Mild cognitive impairment (MCI) is common in those over 70 years old, and half of the cases go on to develop AD. In a trial of 271 elderly people with MCI, a combination of vitamin B6, B12, and folic acid reduced brain matter shrinkage, which is tied to poorer cognitive function .
A follow-up study by the same researchers revealed that the B vitamins were only effective in those people who got enough omega-3 fatty acids in their diets, which highlights how nutrients seem to work together in synergistic ways .
More research on these nutrients is needed.
Based on their experiments, curcumin was hypothesized to inhibit the formation of beta-amyloid deposits, reduce the phosphorylation of tau proteins, bind copper, lower cholesterol, improve microglial activity, inhibit acetylcholinesterase, and improve the action of insulin [68, 69].
However, a review of human studies found no benefits – possibly due to curcumin is poorly absorbed in the digestive tract .
Some scientists argue that another answer could be that curcumin alone is not effective enough .
Curcuminoids are the phenolic constituents of turmeric root. While curcumin is the most important one, others such as demethoxycurcumin and bisdemethoxycurcumin, might also matter. Therefore, some scientists think further research should focus on the whole turmeric root. This theory remains unproven, though .
Ginkgo biloba has long been a popular supplement for Alzheimer’s disease, but no solid evidence supports its use in this population. It has been suggested to improve blood flow in the brain, reduce oxidative damage, and increase levels of the “memory” neurotransmitter acetylcholine .
However, a large study funded by the National Institutes of Health found no effect of ginkgo in preventing or delaying Alzheimer’s disease in over 3000 people. What’s more, data from the same study showed that ginkgo did not slow cognitive decline, lower blood pressure, or reduce the incidence of high blood pressure .
Smaller trials had some positive results, but they are far less reliable. For example, in a smaller trial of 410 patients with Alzheimer’s disease or vascular dementia, 240 mg/d Ginkgo biloba improved cognitive function, mood, and daily functioning. Another study of 404 patients found similar results [73, 74].
Ginkgo biloba (240 mg/d) also improved mood and cognitive function in a small trial of 160 patients with mild cognitive impairment, a state that precedes Alzheimer’s disease .
Some researchers are also studying if Ginkgo biloba inhibits the formation of beta-amyloid deposits, the hallmark of Alzheimer’s disease, in cells and rodents .
No clinical evidence supports the approaches listed in this section in people with Alzheimer’s disease.
Below is a summary of the existing animal and cell-based research, which should guide further investigational efforts. However, the studies listed below should not be interpreted as supportive of any health benefit.
Aside from sugars, the brain can also use fats for fuel. The body breaks down fats into ketone bodies, which are popularly said to “power the brain.” But what does the research say?
Medium-chain triglycerides, such as those in coconut oil, have been hypothesized to improve memory performance in Alzheimer’s disease patients. A ketone body called beta-hydroxybutyrate is claimed to be responsible for cognitive enhancement but proper clinical trials are lacking [77, 78].
Fasting, intermittent fasting, the ketogenic diet, or exercise are purportedly ways to enter ketosis and supplement the brain’s normal reliance on glucose. These interventions have not yet been researched in humans, let alone Alzheimer’s patients .
One unproven theory says that, by putting the mitochondria into higher gear, ketosis decreases oxidative damage in the brain and increases energy release from brain cells. Researchers are investigating whether it can increase the “master antioxidant” glutathione in hippocampal cells (which store memory) and reduce glutamate toxicity [80, 81].
Human studies are needed.
In mice models of Alzheimer’s, MitoQ prevented cognitive decline, neuronal loss, injury from free radicals, and beta-amyloid buildup. In another study of mice with Alzheimer’s, it improved spatial memory [82, 83].
In worms with Alzheimer’s genes, MitoQ extended lifespan by 14% by protecting the mitochondria .
Many substances appear to improve symptoms in simple organisms and animals. The majority of them fail further rigorous clinical testing. MitoQ has yet to be researched in people with cognitive impairment
Scientists are investigating whether the following compounds have an impact on Alzheimer’s pathways in animals, cells, or test tubes:
- Gotu Kola: purportedly by preventing neuron death in Alzheimer’s-like cells by reducing the negative effects of beta-amyloid 
- Phytic acid: neutralized free radicals and cell damage 
- LLLT: In animal studies, low-level laser therapy helped degrade beta-amyloid beta while increasing BDNF, cognition, and learning [87, 88]
- Lithium: seemed to protect brain cells and improve cognition in animals with Alzheimer’s disease 
- Apigenin: hypothesized to delay the onset of Alzheimer’s disease via its antioxidant, anti-inflammatory, brain-protective, and cognition-enhancing effects 
- Caffeine: Methylxanthines such as caffeine, theophylline, and theobromine found in coffee, tea, cacao, and yerba mate are being researched in neurodegenerative diseases like Alzheimer’s 
- THC: in a cell-based study, THC reduced beta-amyloid plaques, lowered inflammation, improved mitochondrial health, and helped brain cells survive longer (by decreasing GSK-3B). Have in mind that THC can be addictive and it’s illegal in most US states [92, 93]
- CBD: being studied for protecting brain cells from beta-amyloid toxicity. It also seemed to reduce cognitive deficits in animals [94, 95, 96]
- Hesperidin: improved cognition, mitochondrial function, and antioxidant defense in mice with Alzheimer’s disease 
- Intermittent hypoxia training (brief repeated exposures to moderate lack of oxygen) experimentally protects blood vessels in the brain, potentially improving memory .
Human data on these interventions are lacking.
Additionally, in a study of 60 patients with Alzheimer’s, sodium benzoate (a food preservative and amino acid breakdown inhibitor) improved cognitive function in patients in the early stages of the disease 
- Can Natural Strategies Help Prevent Alzheimer’s Disease?
- Is Alzheimer’s Genetic? The Possible Causes of Alzheimer’s
Though natural remedies cannot cure Alzheimer’s disease, many strategies may slow its progression and improve cognition. Among the best-researched ones are exercise, vitamin E, spices like saffron and turmeric, as well as antioxidants like resveratrol. You should also get enough sun exposure and dietary fish oil. Additionally, consider huperzine A, gingko, green tea, and B vitamin supplements to slow cognitive decline. Melatonin supplements may balance your circadian rhythm, which is especially important if you have Alzheimer’s. It’s best to combine several natural strategies for synergistic effects, as long as they don’t interact. Ketogenic diets and intermittent fasting may also help, though the evidence is limited.