Alzheimer’s disease is a degenerative brain disorder that develops slowly over several years and is commonly diagnosed in people over 65 years old.
It is thought to be a disease of modern unhealthy lifestyle. Nowadays, many people start to experience signs of cognitive decline and have high levels of amyloid plaques (which cause Alzheimer’s) at a much younger age.
In this post, you will read about not only the causes, symptoms and risk factors but also natural ways to prevent and biohack Alzheimer’s.
What Is Alzheimer’s Disease?
Classified as a type of dementia, Alzheimer’s produces progressive memory and behavioral impairments. Alzheimer’s diseases account for most of all diagnosed dementia cases [R].
A rare form called early onset-Alzheimer’s disease can develop in people as young as 30, but only accounts for 4 to 8% of all cases and only affects those with a strong family history of the disease [R].
Alzheimer’s patients generally live 7 to 10 years if diagnosed in their late 60s or early 70s, but only 3 years or less if diagnosed in their 90s [R].
Overall, the living neuron population and subsequent connections between them decrease in critical areas responsible for memory, emotion, and spatial navigation [R].
The rate of global decrease in brain size (brain atrophy) is 2 to 3% per year as compared to 0.2 to 0.5% per year in a healthy individual [R].
Symptoms of Alzheimer’s Disease
- Memory loss and mild confusion, usually mistaken for difficulties associated with normal aging [R]
- At mild stages, people begin to experience few events of short-term memory loss, instances of unexplained wandering, issues with daily activities, repetition of statements, frequently misplacing personal belongings, and difficulty remembering names and faces [R]
- Impairment of demanding activities such as financial transactions, judgment, problem-solving, or critical thinking; usually depending on someone’s assistance [R]
- Moderate stages show increased functional impairment and lack of independence for complicated tasks. Patients consistently have difficulty remembering new information, often become disoriented, and are unable to recognize close family members [R]
- Advanced stages present behavioral changes such as uncontrollable sporadic temper tantrums, aggression, anxiety, paranoid delusions, and hallucinations [R]
- At the most severe stages, patients ultimately develop a severe loss of mental function due to the degeneration of brain cells (neurons). All patients are completely dependent on a caregiver and can only communicate with simple words or phrases [R]
Causes of Alzheimer’s Disease
Alzheimer’s disease is due to excessive neuronal damage through a complex interaction of the different neuronal stressing factors. Since it is still unclear what the underlying cause of the disease is, researchers only know the essential hallmarks that represent the disease [R].
1) Beta-amyloid Plaque Deposits Block Brain Connections and Signals
Beta-amyloid protein is regarded as one of the hallmarks of Alzheimer’s disease after its discovery in patients in the form of highly concentrated plaques.
Its primary function has yet to be identified, but evidence suggests beta-amyloid has minor functions in many neuronal activities at lower concentrations [R].
Healthy brains facilitate proper degradation and removal of beta-amyloid proteins before apparent plaque formation. However, Alzheimer’s patients lack the proper removal process causing pathological plaque deposits [R].
Plaque deposits form between nerve cells (neurons) causing the connection between neurons to fade and signals in the brain to weaken. These plaque deposits induce many forms of stress that ultimately trigger cell death mechanisms in affected neurons [R].
Drugs that remove amyloid were able to drop amyloid plaque down to normal levels with small insignificant benefits towards mental function. Unfortunately, these studies (as of late 2016) failed to:
- Support or deny the “amyloid hypothesis”
- Show reversible effects of Alzheimer’s disease
- Show if these drugs halt mental decline
Beta-amyloid drugs (aducanumab, verubecestat, etc.) successfully targeted beta-amyloid cleaving peptides (BACE1), which produce beta-amyloid. However, current results do not show if the clinical progression of Alzheimer’s disease is affected by these drugs [R, R].
Studies on these drugs have small sample sizes, and roughly a quarter of the subjects dropped out due to side effects. New results are expected to be released in 2018-2019 [R].
Unfortunately, verubecestat was pulled from further studying in mild-to-moderate Alzheimer’s patients because of efficacy issues. This does not disprove the amyloid hypothesis since the timing of treatment and target mechanisms of the drug may be a crucial factor [R].
Also, aducanumab is progressing towards larger trials with promising results. This may truly confirm or end the amyloid hypothesis.
2) Tau Protein Tangles Cause Death of Neurons
Tau proteins are the second hallmark of Alzheimer’s disease appearing in the form of hair-like neurofibrillary tangles (NFT). These proteins are an important component of the structure and transport systems within neurons [R].
Improper activation of Tau proteins leads to a cascade of neuronal events. Inside of neurons, these events impair the structural integrity of neurons and prevent transport of nutrients across the cell leading to its eventual death [R].
3) Low Levels of Acetylcholine Reduce Neuronal Functions
Acetylcholine is a neurotransmitter responsible for processing learning and memory-related functions in the brain.
A decrease of acetylcholine receptors decreases the sensitivity of neurons. Acetylcholine disperses too rapidly for the weakened neurons to receive the signal [R].
4) Excess Glutamate Becomes Toxic to Neurons
Overactive glutamate produces toxic stress on neurons associated with learning and memory. Glutamate is the major excitatory neurotransmitter for almost all functions in the brain and spinal cord [R].
Chronic mild activation of NMDA receptors by glutamate ultimately leads to neurodegeneration. Prolonged traffic of calcium ions into neurons through NMDA receptor channels overloads synaptic function [R].
Increased levels of the NMDA receptor subunit GluN2B, which enhances cognition while its dysfunction contributes to Alzheimer’s [R].
Evidence currently points at problems with glutamate reuptake and recycling mechanisms. Improper transport of glutamate occurs at higher levels in elderly Alzheimer’s patients when compared to healthy elderly people [R].
5) Inflammation Damages the Brain
The inflammatory process targets injured tissues for repair by the body’s immune system. Inflammation mechanisms remove afflicted areas by destroying injured tissues and already dead cells [R].
Misfolded beta-amyloid proteins bind to microglia and astroglia cells, the support cells of neurons, triggering chronic neuroinflammatory response linked to the progression and severity of Alzheimer’s disease [R].
In a healthy person, microglia protects the brain from pathogens while also maintaining proper balance in the surrounding tissue. However, in Alzheimer’s, microglia produce proinflammatory molecules as a neuroprotectant in response to tau and beta-amyloid, but chronic activation ends up harming neurons [R].
In an Alzheimer’s disease mouse model, these supportive cells react to plaque buildups, fundamentally changing all aspects of their shape, population density, and related functions. These changes cause neurotransmitter imbalances and neural connection problems [R].
There is a growing body of evidence that points to ion channels on microglia as contributing to Alzheimer’s disease. Excessive microglia cells activation and production of toxic molecules, mediated by ion channels, may become targets for disease treatments [R].
6) Infections May Potentially Cause Alzheimer’s Disease
It is suggested that chronic viral infections by virus, bacteria, and fungus might cause inflammation leading to Alzheimer’s. It’s thought that brain or systemic infections may contribute to the development of Alzheimer’s, and chronic infections with several pathogens should be considered a risk factor. The following have been associated with Alzheimer’s [R, R]:
- Human herpesvirus 1 and 2 (HHV-1/2)
- Cytomegalovirus (CMV)
- Borna disease virus
- Chlamydia pneumoniae
- Helicobacter pylori
- Borrelia spirochetes
- Porphyromonas gingivalis and Treponema denticola (cause chronic periodontitis)
The hypothesis that Alzheimer’s disease is caused by infections has been widely studied in both humans and experimental animal models. While the evidence in the literature to confirm that infections actually cause Alzheimer’s is inconclusive, the amount of evidence is too substantial to ignore [R].
For example, bacteria and spirochetes are activators of proinflammatory cytokines, generate free radicals, nitric oxide, and further induce cell death (apoptosis). Recent studies have revealed that exposure to these microorganisms induces beta-amyloid accumulation and tau protein phosphorylation [R].
Also, Borrelia (the bacteria that causes Lyme disease) spirochetes were observed in an autopsy brain tissue from a patient with Alzheimer’s disease. Borrelia species may invade the brain (neuroborreliosis), remain latent for many years, and cause dementia and Alzheimer’s disease [R].
Moreover, fungal DNA has been found in brain samples from Alzheimer’s disease patients [R].
Herpes Simplex Virus Type-1 and Alzheimer’s Disease
While the implications of infections still need to be addressed, there is strong evidence showing that recurrent herpes simplex virus type-1 (HSV-1) infection is a risk factor for Alzheimer’s although the underlying mechanisms aren’t fully understood yet [R].
HSV1, along with the type 4 allele of the apolipoprotein E (APOE) gene, has been linked to Alzheimer’s disease. The virus is normally latent in many elderly brains but reactivates periodically under stress, decreased immunity, and infections. Reactivated HSV1 causes inflammatory damage, involving increased beta-amyloid and tau. Acyclovir (an anti-viral) is effective in reducing HSV1-induced Alzheimer’s-like changes in cell cultures [R, R].
Risk Factors for Alzheimer’s
The greatest risk factor for Alzheimer’s disease is an individual’s age, as late-onset makes up the majority of all cases and affects people over 65 years old [R].
2) Family History
Due to the late onset of Alzheimer’s disease, many of its genetic components are easily passed on before the disease causes severe mental damage.
Someone with a sibling or parent (first-degree relative) diagnosed with Alzheimer’s disease has a higher risk, and it increases with the number of diagnosed family members [R].
Genetic tests are available to determine if you are carrying one of the several genes that increase the risk for Alzheimer’s [R].
Smoking increased more than 100% the risk of Alzheimer’s disease, as well as other types of dementia. Aside from the other health consequences of smoking, heavy smoking during midlife (40-55 years old) greatly increases the risk of Alzheimer’s disease [R].
4) An Unhealthy Lifestyle and Poor Diet
5) Traumatic Brain Injuries
Disruptions of brain function through moderate or severe injury to the head have been shown to increase the risk of developing Alzheimer’s disease [R].
People who experience consistent head injuries due to their profession, such as football athletes, are four times more likely to develop a neurodegenerative condition [R].
6) Poor Sleeping Habits
Sleep deprivation has a strong connection with a greater accumulation of beta-amyloid plaque deposits. As more plaques form, they promote sleep disorders and wakefulness, further progressing Alzheimer’s and other neurodegenerative diseases [R].
Patients in the early stages of Alzheimer’s disease with poor sleep quality and proper sleep quantity had more beta-amyloid plaque deposits. This signifies the importance of sleep quality over sleep quantity in reducing Alzheimer’s disease progression [R].
Stroke is when oxygen doesn’t reach a particular portion of the brain due to a blockage. When oxygen flow is cut off, brain cells start to die after a few minutes causing lasting often permanent brain damage.
Stroke is strongly associated with Alzheimer’s disease in elderly individuals. High risk or history of stroke may lead to an earlier age of onset [R].
Both stroke and Alzheimer’s are common disorders of aging. A meta-analysis showed that stroke can independently and significantly increase the risk of Alzheimer’s disease. Alzheimer’s disease does the same for the risk of stroke [R].
8) Insulin Resistance
Normally, insulin is removed by cells signaling them to uptake glucose from the bloodstream. When the body increases insulin resistance, the body maintains a higher concentration of insulin for longer periods after a meal.
Doctors prescribe insulin injections to treat symptoms of type 2 diabetes, but the evidence is showing a strong link between high concentrations of insulin in the brain and the development of Alzheimer’s disease [R].
Insulin is involved with trafficking beta-amyloid and interfering with its degradation. Abnormal insulin levels also produce synaptic failure and memory decline [R].
9) Increased CRH and Stress
Stress contributes to the development of Alzheimer’s disease. Modern-life stress affects the neurons (reduces the number of dendritic spines in the hippocampus) in an Alzheimer’s-disease mice model. Corticotropin-releasing hormone (CRH) stimulates the amyloid precursor protein (APP) to produce beta-amyloid deposits, which negatively affects dendritic spines [R].
CRH is significantly reduced in the brain (cortex) of Alzheimer’s patients and this decrease is accompanied by increases in CRH receptors in the affected areas, decreasing the activity of the enzyme that produces acetylcholine (ChAT). While the clinical consequences of the changes in CRH are unclear, future therapies directed at increasing CRH levels in the brain may prove useful for treatment [R].
An animal model of Alzheimer’s showed that these mice are more vulnerable to chronic social stress and that such chronic stress exacerbates beta-amyloid accumulation and impairs communication in the brain (neurotrophic signaling). Mice showed increased anxiety, elevated levels of beta-amyloid (also inside the neurons), and decreased BDNF levels [R].
10) Low Testosterone
Increasing evidence indicates that testosterone decreases with age in older men and in postmenopausal women. Treatment with testosterone increases amyloid precursor (APP) and decreases beta-amyloid productions by neurons. These results raise the possibility that testosterone supplementation in elderly men may protect against Alzheimer’s [R].
Low testosterone level worsens cognitive function in elderly men. A meta-analysis showed that low testosterone levels were also significantly associated with an increased risk of Alzheimer’s disease in elderly men [R, R].
11) Aluminum in Drinking Water
Aluminum is toxic to neurons and potentially causes Alzheimer’s disease, particularly in drinking water [R].
A total of 1,925 subjects exposed to aluminum in drinking water showed that cognitive decline and dementia was greater in subjects with a higher daily aluminum intake. Conversely, an increase in silica intake was associated with a reduced risk of dementia. Therefore, high consumption of aluminum from drinking water may be a risk factor for Alzheimer’s disease [R].
Aluminum may play a crucial role in Alzheimer’s development as a cross-linker in beta-amyloid production [R].
Genes Linked to Alzheimer’s
1) Apolipoprotein E-ε4
Apolipoprotein E (ApoE) functions as a cholesterol transporter and assist in injury repair mechanisms in the brain. ApoE also maintains proper digestion of the beta-amyloid protein between neurons [R].
ApoE-ε2 is a rare copy of the Apolipoprotein E gene which reduces the risk of Alzheimer’s or even delays the onset of the disease. ApoE-ε2 has a strong neuroprotective effect with efficient removal of fat-based products such as beta-amyloid protein in critical areas of the brain [R].
ApoE-ε3 is the common copy of the Apolipoprotein E gene and does not have any positive or negative role in the disease’s pathology [R].
Meta-analyses of the ApoE-ε4 copy, however, show that the ApoE-ε4 copy is a major risk factor for Alzheimer’s disease in all ethnic groups studied [R].
ApoE-ε4 is less efficient in proper clearance of beta-amyloid protein when compared to ApoE-ε2 and ApoE-ε3 allowing for the buildup of plaques between neurons [R].
Carriers of one or more ApoE-ε4 copies may begin to experience Alzheimer’s disease associated brain changes as early as middle age [R].
2) Presenilin Gene Mutation
Mutations in the PSEN1 is one of the most common mutations associated with earlier and more aggressive forms of Alzheimer’s disease. Onset can occur as early as age 30 with patients developing severe neuronal loss, plaque formations, and neurofibrillary tangles [R].
3) Other Genes
NOS2 (Nitric Oxide Synthase 2) is responsible for fueling the brain with an important transmission and repair molecule called nitric oxide. Those with Alzheimer’s have higher concentrations of nitric oxide which is toxic for neurons [R].
CASP3 (Caspase 3) is necessary for brain development and also helps to signal programmed cell death (apoptosis). CASP3 has been implicated in mechanisms involving neurodegeneration in Alzheimer’s disease [R].
Also, the association between Alzheimer’s disease and pesticides may be stronger among genetically susceptible individuals. A study of 200 people found that GSTP1 may be a candidate gene for Alzheimer’s since some variants (B and C) increased its risk. Also, some variants of CYP2D6 and GSTP1 genes may interact with pesticides (beta-hexachlorocyclohexane, dieldrin, and copper) increasing the risk of Alzheimer’s [R].
Prevention of Alzheimer’s Disease
Research on the prevention of Alzheimer’s disease is not yet convincing. Since Alzheimer’s is such a complex disease, there is no current proven method to prevent it.
However, diabetes and heart disease have strong links to Alzheimer’s, which is prevented through diet and exercise. The main idea is that living a healthy lifestyle with good nutrition and physical activity is critical [R, R, R, R, R].
1) Formal Education
Years of education builds a more complex set of connections between neurons in the brain, called a “cognitive reserve” [R].
2) Increased Social and Mental Activity
It is important to keep your brain active as much as possible through social interaction and other mentally stimulating activities especially later in life. Keeping your brain active can reduce the risk of Alzheimer’s disease if it runs in your family [R].
3) Live a More Ancestral Lifestyle
Alzheimer’s is a modern-day disease and has only begun to rise in recent decades [R].
Third world countries with difficult access to food like Africa, India, and South Asia have the lowest rates of Alzheimer’s disease while Western Europe and North America have the highest [R].
Genetic factors play a very insignificant role in late-onset sporadic Alzheimer’s disease cases. Africans have significantly lower incidences of Alzheimer’s while African-Americans have 5x higher rates [R].
People who move to Western countries and adopt their diet/lifestyle have their Alzheimer’s rates increased dramatically [R].
Moreover, countries like Japan that are starting to adopt Western food/lifestyle habits are increasing the rates of dementia and Alzheimer’s disease [R].
Cardio exercises (aerobic) reduce the risk of cognitive impairment and dementia [R].
5) The Mediterranean Diet
The Mediterranean diet consists of foods traditionally consumed in cultures surrounding the Mediterranean sea. It focuses on fruits, vegetables, spices, healthy fats (olive oil), and seafood as its main protein source.
Higher adherence to the Mediterranean diet is significantly related to a reduced risk of Alzheimer’s disease [R].
Moreover, those with higher adherence to the Mediterranean diet have decreased mortality risk due to Alzheimer’s disease [R].
A recent study on 24,325 participants has also shown that the Mediterranean diet is associated not only with lower inflammations but also with a reduced blood clotting (due to a decrease in D-dimer levels) [R].
6) Methylene Blue
Methylene blue may slow down the progression of Alzheimer’s. Methylene blue attenuates the formation of amyloid plaques and neurofibrillary tangles and repairs mitochondrial impairments. Furthermore, acetylcholine, serotonin, and glutamate are also influenced by methylene blue [R].
Methylene blue is one of the most effective agents to delay aging in normal human cells and it can also delay the onset of Alzheimer’s. It stimulates mitochondrial function by increasing hemoglobin transport, cytochrome c oxidase, and mitochondrial energy production (respiration), which are impaired in the brains of patients with Alzheimer’s [R].
In animal studies, methylene blue also reduced beta-amyloid levels and improved early cognitive decline (by increasing proteasome activity) [R].
7) Sirtuins, NF-kB, and Polyphenols
Sirtuins are enzymes that have beneficial effects against age-related diseases like Alzheimer’s. In most of these studies, it has been found that increased SIRT1 has protective effects. Therefore, treatments based on SIRT1 activity might be important to investigate [R].
Cell-based studies have shown that SIRT1 attenuates the conversion of amyloid precursor (APP) to beta-amyloid deposits in a mouse model of Alzheimer’s [R].
NF-κB is one of the key mediators of aging and is activated by toxic, oxidative, and inflammatory stresses. In mouse models, inhibition of NF-κB leads to delayed onset of age-related symptoms and disorders. Thus, NF-κB represents a possible therapeutic target for extending mammalian healthspan [R].
Scientific evidence suggests that dietary polyphenols such as resveratrol, epigallocatechin-3-gallate (EGCG), and curcumin have the capacity to mitigate age-associated cellular damage induced by reactive oxygen species (ROS) by increasing the activity of SIRT1 [R].
More recently, polyphenols have been also shown to reduce the production of beta-amyloid and modulate cell communication and sirtuin proteins [R].
Potential Pharmaceutical Treatments for Alzheimer’s Disease and Their Limitations
There is no cure for Alzheimer’s disease. Researchers have yet to identify a singular underlying cause that triggers the progression of the disease.
Established pharmaceutical treatments only target Alzheimer’s disease symptoms to improve the patient’s quality of life. Scientists are debating whether the amyloid plaque or the tau protein hold the key to a potential cure.
With further research, scientists might create a combined drug therapy that targets both underlying causes of Alzheimer’s disease [R].
1) Cholinesterase Inhibitors
Acetylcholine has a major role in learning and memory. Cholinesterase inhibitors (ChEI) block the breakdown of acetylcholine increasing its levels in the brain.
By sustaining acetylcholine levels, cholinesterase inhibitors can compensate for the loss of functioning brain cells [R].
In a study (DB-RCT), 207 patients with moderate Alzheimer’s disease experienced benefits in mental capacity, increased activities of daily living, and a more positive emotional state with a cholinesterase inhibitor (donepezil) compared to placebo [R].
Memantine, an NMDA receptor blocker, protects neurons from the toxic effects of overactive glutamate release (glutamate-induced excitotoxicity) produced by the effects of Alzheimer’s disease.
Glutamate is the main excitatory neurotransmitter responsible for interneuronal communication within virtually every region of the brain. Prolonged exposure to glutamate causes overstimulation of cell-surface receptors and ultimately neuronal death [R].
At low concentrations, memantine promotes and preserves brain development while reducing the progressive neuronal loss underlying Alzheimer’s disease [R].
Natural Treatments for Alzheimer’s Disease
1) Vitamin E
There is clear evidence showing the oxidative damage caused by Alzheimer’s disease. Hence, antioxidant therapy became a potential treatment [R].
Antioxidant therapy is still in its early stages with only vitamin E showing promising results. Other popular antioxidants (vitamin C, beta-carotene, etc.) cannot cross the blood-brain barrier and will have no direct effect on the brain. The next step is to search for an ideal antioxidant or a transport system for current antioxidants to cross the brain barrier [R].
A study (DB-PCT) showed that saffron is both safe and effective in mild-to-moderate Alzheimer’s. Saffron significantly improved cognitive function compared to placebo, that at least in the short-term [R].
Moreover, a study (DB-RCT) of 54 patients with Alzheimer’s showed that saffron (Crocus sativus) is as effective as donepezil (a cholinesterase inhibitor) in the treatment of mild-to-moderate Alzheimer’s. The frequency of adverse effects was similar between both treatments with the exception of vomiting, which occurred significantly more frequently in the donepezil group [R].
Research shows that vitamin E, turmeric, and saffron are alternative antioxidant therapies able to protect neurons against free radical damage, moderate acetylcholinesterase (an enzyme involved in the breakdown of acetylcholine) activity, and reducing neurodegeneration, which are key factors in Alzheimer’s [R].
3) Turmeric (Curcumin)
A review of scientific literature shows that curcumin (the main active component of turmeric) can both prevent and treat Alzheimer’s disease. Curcumin as an antioxidant, anti-inflammatory, and lipophilic action improves cognitive functions. It decreases beta-amyloid plaques, delays degradation of neurons, chelates heavy metals, and improves overall memory in patients with Alzheimer’s [R].
Curcuminoids, a mixture of curcumin, demethoxycurcumin, and bisdemethoxycurcumin, are vital constituents of turmeric. While curcumin is the most important constituent, the other two constituents also contribute significantly to the effectiveness of curcuminoids in Alzheimer’s. Therefore, the curcuminoid mixture is better than curcumin alone [R].
It was also shown that curcumin inhibits the formation and promotes the disaggregation of beta-amyloid plaques, attenuates the hyperphosphorylation of tau and enhances its clearance, binds copper, lowers cholesterol, modifies microglial activity, inhibits acetylcholinesterase, and mediates the insulin effects [R].
In conclusion, curcumin has the potential to be more effective than many current treatments. However, its usefulness as a therapeutic agent may be hindered by its low bioavailability, which still has to be figured out.
4) Physical/Leisure Activity for The Elderly
The direct effect of increased physical activity in the human brain is still under investigation, however, studies using mice suggest a decreased rate of plaque formation in the brain with increased physical activity [R].
Patients with Alzheimer’s who go on walks regularly have reduced depression and have enhanced the performance of daily activities [R].
Resistance training improves balance, mobility performance, and reduces falling risk in people with Alzheimer’s. Resistance exercise programs combine strengthening and walking exercises [R].
5) Increased Mental Activity
Mental activity can prevent or delay the onset of Alzheimer’s disease and other cognitive disorders of aging. Heightened mental activity increases neuron connections, brain volume, and integrity of white matter all of which fight against Alzheimer’s disease [R].
Reading, playing games, and even dancing are great mentally challenging activities that help elderly people stay sharp [R].
Studies showing that memory practice and cognitively stimulating activities treat Alzheimer’s disease, more research is still needed to confirm the biological aspects of the increased mental activity method.
Despite common belief, the brain does not only use sugar as its source of fuel. Instead, fats (from the body or food) can be broken down into ketone bodies to power the brain.
Fats (medium-chain triglycerides) in supplements like coconut oil improve memory performances in Alzheimer’s disease patients. A ketone body, beta-hydroxybutyrate, is responsible for improved cognitive ability [R, R].
Fasting, intermittent fasting, the ketogenic diet, or exercise are great ways to make the body enter ketosis in order to supplement the brain’s normal reliance on glucose [R].
Ketosis decreases oxidative damage in the brain while increasing greater neuronal cellular energy output by increasing mitochondrial efficiency. Glutathione is also increased in hippocampal cells and glutamate toxicity is reduced [R, R].
7) Sun Exposure
Patients with Alzheimer’s were exposed to bright light significantly less than healthy controls. Healthy elderly received about two-thirds the duration of bright light received by healthy younger subjects [R].
There is an association between decreased exposure to bright light and the declines in sleep quality, which is also a risk factor for Alzheimer’s [R].
People with Alzheimer’s had disturbed circadian rhythms [R].
Red to infrared light therapy (λ = 600 – 1070 nm), and in particular light in the near infrared range, is capable of arresting neuronal death. This therapy is being explored for Alzheimer’s patients [R].
Increased light exposure consolidates sleep and strengthens circadian rhythms in severe Alzheimer’s disease patients [R].
The use of synthetic melatonin analogs or melatonin-related molecules to block nitric oxide synthase are being evaluated for the treatment of neural diseases like Alzheimer’s [R].
In mouse nerve cells, melatonin prevented cell death caused by amyloid beta 25 – 35, a substance that causes a condition similar to Alzheimer’s disease [R].
The decrease in melatonin may explain in part the disruption of sleep and problems with processing information observed in Alzheimer’s patients [R].
In an animal model of Alzheimer’s, melatonin’s antioxidant effects were more efficient than vitamin C and E in treating the disease and reducing oxidative stress [R].
9) Huperzine A
By decreasing the inflammatory response triggered by beta-amyloid, Huperzine A could stop cell death (apoptosis) [R].
A clinical trial has shown that Huperzine A improved mental ability and overall well-being in some patients with Alzheimer’s disease [R].
10) Vitamin D
Blood levels of vitamin D less than 50 nmol/L were associated with a higher risk of Alzheimer’s disease and dementia [R].
A meta-analysis (17 studies, 2,090 subjects) showed that patients with Alzheimer’s had significantly reduced blood manganese levels. Therefore manganese deficiency may be a risk factor for Alzheimer’s, but the causal proof is still missing [R].
It can also improve spatial memory in mice models of Alzheimer’s [R].
In worms with Alzheimer’s genes, MitoQ extended lifespan by 14%, by protecting the mitochondria [R]. However, it did not do so in normal worms.
Alzheimer’s Disease causes the brain to use glucose less efficiently. Phosphatidylserine supplementation improved glucose metabolism in brains affected by this condition [R, R].
14) Potassium Intake
Increased potassium intake leads to a change in the aggregation of beta-amyloid in brain tissues, improvement in cognitive performance, and a decrease in markers related to inflammation and oxidative stress (R).
15) Olive Oil
Mice that had memory loss had olive oil included in their diet for eight weeks. Their memory improved, and there was a significant response in the cortex to promote the formation of new cells in the brain. The continuous intake of olive oil may prevent or delay Alzheimer’s [R].
Alzheimer’s is characterized by the accumulation of beta-amyloid and tau proteins in the brain. In mice, olive oil leads to an up-regulation of beta-amyloid degrading enzymes [R].
Other Potential Natural Treatments
- Gotu Kola: Gotu Kola prevents neuron death in test-tube models of Alzheimer’s by reducing the negative effects of beta-amyloid [R]
- Phytic acid: In a cell-based study, phytic acid protected against an amyloid precursor toxicity by decreasing the levels of calcium inside the cells, free radicals (hydrogen peroxide and superoxide), beta-amyloid, and cell damage (autophagy) [R]
- LLLT: In animal studies, low-level laser therapy (LLLT) showed to increase degradation (phagocytosis) of beta-amyloid beta and increased BDNF improving cognitive capacity and spatial learning [R, R]
- Lithium: Lithium has been shown to protect the neurons and improve behavioral and cognitive deficits in animal models of Alzheimer’s disease [R]
- Sodium benzoate: A study (DB-PCT) of 60 patients with Alzheimer’s showed that sodium benzoate (a food preservative and amino acid breakdown inhibitor) improved cognitive and overall functions in patients with early stages of the disease [R]
- Apigenin: A review showed that, due to its antioxidant, anti-inflammatory, anti-amyloid, neuroprotective, and cognition-enhancing effects, apigenin might delay the onset of Alzheimer’s disease [R]
- Caffeine: Methylxanthines such as caffeine, theophylline, and theobromine found in coffee, tea, cacao, and yerba mate may potentially prevent and even treat neurodegenerative diseases like Alzheimer’s [R]
- THC: Although the use of THC in brain disorders is still controversial, a cell-based study showed that THC, through cannabinoid receptors, interact with beta-amyloid inhibiting the plaque deposits, lower protein degradation and cell death (by decreasing GSK-3B), enhance mitochondrial function, and decrease inflammation, which can potentially treat Alzheimer’s disease [R, R]
- CBD: CBD oil may also protect brain cells from beta-amyloid toxicity, making it a potential therapeutic agent in Alzheimer’s disease. CBD has been shown to reverse cognitive deficits in animal models [R, R, R]
- Hesperidin: An animal study showed that hesperidin improved cognitive impairment and mitochondrial dysfunction through the inhibition of GSK-3B activity and increased antioxidant defense in a mouse model of Alzheimer’s disease [R]
- Intermittent hypoxia training (brief repeated exposures to moderate lack of oxygen) protects the function of the blood vessels in the brain improving memory in Alzheimer’s disease patients [R].
- Resveratrol: The polyphenolic compound resveratrol protected the neurons in animal models of Alzheimer’s due to its antioxidant effects [R]