Emerging research gives us clues about the best ways to naturally stop Alzheimer’s disease in its tracks or slow it down. Read on for a full breakdown of lifestyle changes, supplements, dietary approaches that may help.
We currently don’t have a cure for Alzheimer’s disease (AD). However, we don’t really have a cure for most chronic diseases.
Alzheimer’s disease sounds like the worst thing you could be diagnosed with. In truth, many targeted natural strategies outlined below can improve your brain health and potentially slow the disease down.
Even if you don’t have Alzheimer’s disease, these strategies are important for enhancing brain health. 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 [1, 2, 3, 4].
Review studies show that exercise can help patients with Alzheimer’s disease. It improves cognitive function, boosts mood, and slows the rate of decline in the patient’s ability to take care of themselves [5, 6, 7, 8, 9, 10].
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 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 trial of 26 people. A physical training program also improved balance, mobility, and reduced the risk of falling in 40 patients with Alzheimer’s [12, 13].
Interestingly, rodent studies show that physical activity leads to a decreased rate of beta-amyloid formation in the brain, a major factor of Alzheimer’s disease .
Exercise can help improve the symptoms of Alzheimer’s disease. It enhances memory, mood, and mobility.
Research in animals and cells shows that antioxidants such as vitamin E, turmeric, and saffron can protect neurons against free radical damage, restore acetylcholine levels to normal, and prevent the formation of beta-amyloid deposits. Acetylcholine is the most important neurotransmitter for memory and learning .
An observational study of ~5,400 people found that higher intakes of vitamin E were associated with lower rates of dementia, including Alzheimer’s disease .
In a trial of 613 patients with mild-to-moderate Alzheimer’s, vitamin E at a dose of 2,000 IU/d slowed down disease progression and functional decline, more than memantine or placebo .
However, a trial of 341 patients with moderate Alzheimer’s disease found that either selegiline or vitamin E (2,000 IU/d) could slow the progression of the disease .
Unfortunately, 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 a 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 study may have failed because the dose of vitamin E was too low .
Moreover, a study of 54 patients showed that saffron is as effective as donepezil (a cholinesterase inhibitor) at treating the symptoms of mild-to-moderate Alzheimer’s disease. The side effects were similar between both treatments with the exception of vomiting, which occurred significantly more often in the donepezil group .
Saffron may improve cognitive function in mild-to-moderate Alzheimer’s disease with fewer side effects than pharmaceuticals.
Curcumin inhibits the formation of beta-amyloid deposits, reduces the phosphorylation of tau proteins, binds copper, lowers cholesterol, improves microglial activity, inhibits acetylcholinesterase, and improves the action of insulin [22, 23].
However, a review of human studies found no benefits – possibly due to curcumin is poorly absorbed in the digestive tract .
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, are also vital. Therefore, the whole turmeric root might be more effective than curcumin alone .
Curcumin may improve Alzheimer’s disease. However, it has poor bioavailability. Whole turmeric root might be more effective.
In a trial of 119 patients with mild-to-moderate Alzheimer’s disease, 500-2,000 mg resveratrol halted 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, which is bad news for those of us carrying this mutation. The dosage was relatively low, at 150 mg daily .
Interestingly, patients who received resveratrol also had lower rates of cancer. This could mean that targeting SIRT1 protects not only against Alzheimer’s, but also other age-related diseases .
Besides activating SIRT1, resveratrol may also work by improving autophagy. Autophagy breaks down and recycles diseased and damaged cells. In Alzheimer’s disease, autophagy is impaired, and improving it could help prevent or treat the disease .
Resveratrol may slow or halt the progression of Alzheimer’s disease, but only in high doses (> 500 mg) and in non-ApoE4 carriers.
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. Alzheimer’s disease patients have low melatonin, which may partly explain the disruption of sleep and cognitive function .
A study of 18 people also found 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 .
People with mild cognitive impairment, the precursor state to dementia, may also benefit from melatonin. 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 [37, 38].
In animal models of Alzheimer’s disease, melatonin was more effective than vitamin C and E in improving symptoms and reducing oxidative stress .
In a cell-based study, melatonin prevented cell death caused by synthetic beta-amyloid proteins, which are very similar to those that trigger Alzheimer’s disease .
Melatonin at a dose of 2-9 mg/d may improve symptoms and slow the progression of Alzheimer’s disease by balancing the sleep-wake cycle.
Huperzine A is sparking the interest of many scientists as a natural treatment for Alzheimer’s disease, mainly because of its ability to increase acetylcholine levels and improve memory in animals .
Huperzine A improves blood flow in the brain, reduces free radical damage, and protects against excess glutamate. Clinical trials in China have found it improves cognitive function and quality of life in Alzheimer’s disease patients .
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 [43, 44].
By decreasing the inflammation triggered by beta-amyloid proteins, Huperzine A could stop cell death (apoptosis) in a cell-based study .
Huperzine A may improve cognitive function and quality of life in Alzheimer’s disease by increasing acetylcholine levels in the brain.
A review of observational studies revealed Alzheimer’s disease patients 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 [47, 48].
A trial of 52 people revealed that vitamin D reduced beta-amyloid deposits and improved cognitive function, but only in those with a mild cognitive impairment which precedes Alzheimer’s disease. Patients with early Alzheimer’s disease did not experience improvement .
Moreover, cell studies show that vitamin D stimulates immune cells to break down beta-amyloid deposits in the brain. At the same time, vitamin D protects healthy brain cells against damage from beta-amyloid proteins [51, 52].
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 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 [55, 56].
A cell study also revealed that phospholipids including phosphatidylserine inhibit inflammation and the formation of beta-amyloid proteins .
Ginkgo biloba has long been a popular supplement for Alzheimer’s disease. It improves blood flow in the brain, reduces oxidative damage, and increases levels of the “memory” neurotransmitter acetylcholine .
In a 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 [60, 61].
Ginkgo biloba (240 mg/d) also improved mood and cognitive function in a trial of 160 patients with mild cognitive impairment, a state that precedes Alzheimer’s disease .
What’s more, studies in cells and rodents revealed that Ginkgo biloba inhibits the formation of beta-amyloid deposits, the hallmark of Alzheimer’s disease .
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 [65, 66].
Interestingly, an observational study of 1,000 elderly people in Japan found that those with the highest green tea consumption had the lowest rates of cognitive impairment .
Several animal and cell studies have revealed that green tea or its constituent EGCG improve cognitive function, reduce oxidative stress and inhibit the formation of beta-amyloid deposits .
A recent mouse study found that a combination of EGCG and ferulic acid was even more effective at treating Alzheimer’s disease than either compound alone. This combination completely reversed cognitive impairments in the mice .
Green tea may improve Alzheimer’s disease, but clinical trials have shown mixed results. Pure EGCG may be effective, especially in combination with ferulic acid.
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 can work together in synergistic ways .
Interestingly, an observational study of 1,300 people found that those with the highest intake of folate had a reduced risk of developing dementia .
B vitamins may improve cognitive function and slow brain damage in Alzheimer’s disease, particularly when taken with omega-3 fatty acids.
Aside from sugars, the brain can also use fats for fuel. The body breaks down fats into ketone bodies, which can power the brain.
Medium-chain triglycerides, such as those in coconut oil, improve memory performance in Alzheimer’s disease patients. A ketone body called beta-hydroxybutyrate is responsible for cognitive enhancement [75, 76].
Fasting, intermittent fasting, the ketogenic diet, or exercise are great ways to enter ketosis and supplement the brain’s normal reliance on glucose .
By putting the mitochondria into higher gear, ketosis decreases oxidative damage in the brain and increases energy release from brain cells. Plus, ketosis increased the master antioxidant glutathione in hippocampal cells (which store memory) and reduced glutamate toxicity [78, 79].
Ketogenic diets and intermittent fasting may improve memory in people with Alzheimer’s disease by boosting antioxidant defense and mitochondrial function.
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 [80, 81].
In worms with Alzheimer’s genes, MitoQ extended lifespan by 14% by protecting the mitochondria .
The evidence to back up the following natural remedies are weak. Additional studies would bring them further up the list.
If you’re interested in natural and targeted ways of improving your cognitive function, we recommend checking out SelfDecode’s Limitless Mind DNA Protocol. It gives genetic-based diet, lifestyle and supplement tips that can help improve your cognitive function. The recommendations are personalized based on your genes.
We also recommend SelfDecode’s comprehensive guide on the ApoE gene, with recommendations about how to lower risk if you have the risk-associated ApoE ε4 variant.
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Though natural remedies cannot cure Alzheimer’s disease, many strategies can 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.
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