Table of Contents
- What is Alzheimer’s Disease?
- Symptoms of Alzheimer’s Disease
- Causes of Alzheimer’s Disease
- Risk Factors for Alzheimer’s
- How is Genetics Linked to Alzheimer’s?
- How Can I Prevent Alzheimer’s?
- When Should I See a Doctor?
- What are Pharmaceutical Treatments?
- Other Conventional Treatments
- The Future of Alzheimer’s Drug Research
- Natural Treatments for Alzheimer’s Disease
- Other Potential Natural Treatments
What is Alzheimer’s Disease?
Alzheimer’s disease is the most common form of dementia, afflicting 60-80% of people with the illness.
Alzheimer’s can cause problems with your ability to remember, think, and act appropriately.
Alzheimer’s disease usually develops over a long period of time, and symptoms often increase in severity as you age, eventually interfering with normal tasks (1).
While Alzheimer’s usually affects people over 65, you may develop the disease earlier in life (2).
Alzheimer’s disease in the number six cause of death in the US, affecting over five million people currently.
Ten percent of those over 65 in the US have Alzheimer’s disease.
While some survive up to 20 years with the disease, the average person lives eight years from the point where others notice symptoms (3).
Alzheimer’s is believed to be largely a disease of the modern age, and it is predicted that 16 million people could have it by 2050.
Symptoms of Alzheimer’s Disease
Alzheimer’s disease is degenerative, meaning it worsens over time.
The connections between brain cells, called neurons, as well as the brain cells themselves become damaged over time.
The most common symptoms are memory loss and confusion.
Other symptoms of Alzheimer’s include difficulty focusing, difficulty completing ordinary activities, confusion, frustration, outbursts of depression or anxiety, disorientation, becoming lost easily, poor coordination, other physical problems, and communication issues.
As the disease progresses, people will have trouble with problem-solving tasks, keeping track of finances, making important decisions, and exercising judgment.
As symptoms worsen over time, those with Alzheimer’s disease may fail to recognize family and loved ones, may have difficulty swallowing, be paranoid or angry, and require constant care (6).
Causes of Alzheimer’s Disease
We are still learning a great deal about the causes of this degenerative brain disorder.
As technology in imaging, genetics, and medical research advances, so does our understanding of how the brain functions and how diseases like dementia and Alzheimer’s develop.
As this disease affects more and more of our population, we will continue to grow our knowledge of its causes and treatments.
At this time, we can only identify the underlying causes of the neuronal damage that are hallmarks of the disease but do not have a comprehensive understanding of what actually causes it (7).
High concentrations of beta-amyloid proteins are seen in most Alzheimer’s patients’ brains.
These proteins develop into plaque in the neuronal pathways, disrupting brain function.
When your brain is healthy, it degrades and removes beta-amyloid proteins so that they do not form into plaque.
Because this process is disrupted in Alzheimer’s patients, plaque deposits form between nerve cells (8).
When neural connections fade, signals within the brain weaken and cognition slows.
Eventually, these neurons will die from stress and lack of use (9).
There is not enough evidence yet to support whether drugs that reduce or remove beta-amyloid deposits have an impact on Alzheimer’s progression or symptoms.
While trials continue to examine whether beta-amyloid drugs like aducanumab can have an effect on the progression of Alzheimer’s by targeting the beta-amyloid cleaving peptides (BACE1), 2016 results were inconclusive because of sample sizes that were too small (10, 11).
Results of these ongoing studies should be available by 2019 to provide further evidence of the amyloid hypothesis.
The beta-amyloid drug verubecestat, which had been studied previously, was removed from trials in patients with mild-to-moderate Alzheimer’s over efficacy concerns, but aducanumab is still being studied and moving toward larger trials.
This research can hopefully confirm or deny the amyloid hypothesis for Alzheimer’s treatment.
Tau Protein Tangles
Just as beta-amyloid proteins clump into plaque in Alzheimer’s patients’ brains, tau proteins form neurofibrillary tangles (NFT), which impact how the brain functions.
In a healthy brain, tau proteins are an important part of the transport system inside our bodies, moving nutrients, cell parts, and other important materials.
Tau normally helps that transport system by keeping the “tracks” straight.
When tau develops into hair-like bunches called NFT, they block the transportation system and hinder cell development, and then synaptic signals fail (12).
Cells affected by NFT will eventually die from lack of supplies.
Tau protein tangles are the second hallmark of Alzheimer’s disease, and therefore an important area of focus for researchers studying this disorder (13).
Neurotransmitter Difficulties – Glutamate and Acetylcholine
Your brain uses chemicals called neurotransmitters to send signals between neurons.
The most abundant type of neurotransmitter is glutamate, which accounts for over 90 percent of the synaptic connections in our brains.
Glutamate is used to perform nearly every major excitatory function in the human brain (14).
Therefore, it is important that we understand its role in brain diseases such as Alzheimer’s.
When glutamate is overactive, it inflicts stress on neurons, including those responsible for memory and cognition.
Toxic levels of stress mean neurons cannot perform appropriately or may degrade (15).
Neurodegeneration can be caused by the NMDA receptors in our brains being chronically activated by glutamate.
In addition, when GluN2B, a subunit NMDA receptor, is not at appropriate levels, cognition is affected and it contributes to Alzheimer’s development (16).
All current evidence tells us that those with Alzheimer’s usually have problems with recycling and reusing glutamate, as opposed to elderly people without dementia (17).
Acetylcholine is another neurotransmitter that helps with learning and memory in the brain.
When acetylcholine receptors decrease in efficacy, neuronal sensitivity decreases, meaning neurons are too weak to receive incoming signals (18).
More research is needed to understand fully the role of acetylcholine in Alzheimer’s, and how this could result in successful treatment methods.
Your body’s response to injured or dead tissues or cells is called inflammation.
This natural process can be beneficial when it is part of the natural healing process (21).
However, when conditions persist to create chronic inflammation, serious problems can occur.
A healthy brain utilizes microglia to protect against pathogens.
When someone has Alzheimer’s disease, though, the brain detects the tau tangles and beta-amyloid proteins as pathogens and triggers a chronic neuroinflammatory reaction that is responsible for the progression of Alzheimer’s (22).
This chronic activation, which is meant to be a neuroprotectant, actually ends up harming neurons even more.
The inflammation response is responsible for imbalances in neurotransmitter density and function and creates other neural connection issues (23).
The targeting of microglia cell activation processes will likely become the focus of future Alzheimer’s treatment research, as well (24).
Because we already know inflammation is a contributing factor for Alzheimer’s, any disease that produces inflammation can contribute to the development of dementia or Alzheimer’s in the elderly.
Chronic infections, including fungal, viral, and bacterial infections, can cause inflammation in the brain and other systems, contributing to Alzheimer’s progression (25).
Like other types of inflammation already discussed, the microorganisms in certain pathogens accelerate the accumulation of beta-amyloid and tau proteins.
When you have more than one pathogen causing chronic infection, you have a higher risk of developing Alzheimer’s.
Those infections most commonly associated with Alzheimer’s include human herpesvirus 1 and 2 (HHV-1/2), cytomegalovirus (CMV), picornavirus, Borna disease virus, chlamydia pneumoniae, Helicobacter pylori, Borrelia spirochetes (Lyme disease), porphyromonas gingivalis, and Treponema denticola (26).
There is evidence to suggest that infection from the herpes simplex virus type-1 (HSV-1) can lead to changes in cells similar to Alzheimer’s, including the increase of beta-amyloid and tau already discussed (29).
Many elderly may have this virus in their system, but it usually remains latent.
The virus can be reactivated by lowered immunity, stress, and other infections.
Once reactivated, HSV-1 causes inflammation and damage.
Those most affected by HSV-1 will also have the APOE gene, so HSV-1 does not have the same effect on everyone (30).
Researchers are still working fully to understand HSV-1 as a risk factor for Alzheimer’s disease.
Risk Factors for Alzheimer’s
The medical community generally believes that Alzheimer’s disease is caused by a combination of genetics and other risk factors, rather than one single cause.
There are some risk factors we can control our behavior and lifestyle, while others are predetermined.
If you have a family member with Alzheimer’s disease, you have an increased risk for developing the disease as well, particularly if that person is a first-degree relative, such as a mother or brother (31).
As with all diseases with a genetic component, if there are more members of your family with the disease, you are at an increased risk yourself.
However, just because someone you are related to has Alzheimer’s disease does not necessarily mean you will, too.
The information below on the role of genetics in Alzheimer’s will help you determine your risk of developing the disease.
While not everyone will develop Alzheimer’s as a part of the normal aging process, age is the strongest risk factor.
While young-onset Alzheimer’s does exist, it only affects a small portion of the Alzheimer’s population, and the vast majority who develop the disease are older (32).
Your risk of developing Alzheimer’s doubles every five years after you turn 65.
Aging damages your body’s ability to repair itself, and this is true for the brain as well as other systems.
Therefore, it is important to be aware of the symptoms of Alzheimer’s disease and to monitor yourself and the elderly in your life closely.
The heavy smoking long-term, particularly for those between the ages of 40-55, has been known to cause many health issues, and it has now been linked with an increased risk for developing Alzheimer’s disease.
Because smoking increases inflammation, reduces vascular flow, and has other impacts on your health, it is believed it can contribute to the development of dementia, including Alzheimer’s (33).
It is estimated that smoking increases your risk of developing Alzheimer’s to more than 100 times that of a non-smoker.
Stroke and Other Cardiovascular Diseases
There is much evidence to suggest that the health of your heart plays a large role in the health of your brain.
Because your heart sends nourishing blood to all parts of your body, including your brain, when your heart is not performing well, your brain suffers.
Since brain cells cannot grow back once damaged, lasting starvation to the brain for oxygen and nutrients has profound implications.
Any condition that damages the circulatory system increases your risk of Alzheimer’s, including heart disease, stroke, high blood pressure, high blood sugar or cholesterol, and valve problems.
A stroke is when part of your brain is cut off from the supply of oxygenated blood.
If you have had a stroke or damage to the blood vessels that serve your brain, then beta-amyloid plaque and tau tangles are more likely to contribute to the development of Alzheimer’s (34).
In elderly patients, the risk of stroke is high when Alzheimer’s had been diagnosed, and the risk of Alzheimer’s is high after a stroke (35).
Traumatic Brain Injury
Damage to the brain from injury causes disruption in brain function and death to brain cells.
Whether because of the inflammation associated with brain injury, the disruption of neurotransmitters, or other causes, those who have experienced a moderate to severe head injury are at an increased risk for Alzheimer’s disease.
Those who experience consistent brain trauma, such as boxers or other athletes, are much more likely to develop some type of dementia, as neurodegeneration is increased with this type of repetitive injury (36).
Unhealthy Lifestyle and Poor Diet
Your brain’s health is linked to your body’s overall health. When you have conditions that raise levels of inflammation, affect your vascular health, or add unhealthy levels of certain compounds to your blood, it will impact your brain.
Elevated blood sugar increases plaque buildup in your brain, doubling your risk of Alzheimer’s (39).
Choosing to eat fatty and unhealthy foods that impact your heart, pancreas, liver, and lungs will greatly impact your brain.
This is why researchers often call Alzheimer’s a modern-day disease because the prevalence of the disease has risen with the prevalence of the unhealthy diet we see in modern cultures.
Poor Sleep Quality
Increased accumulation of beta-amyloid plaque is seen in brains that are deprived of sleep, especially those with prolonged sleep issues.
As you develop more plaque, your body manifests sleep disorders, contributing to the progression of plaque buildup and worsening diseases such as Alzheimer’s (40).
The quality of your sleep is more important than the amount of sleep you get, so addressing sleep problems such as apnea is important for controlling plaque formation (41).
Eighty percent of those with Alzheimer’s also have insulin resistance or Type 2 diabetes.
This correlation cannot be ignored, so understanding the role of insulin and blood glucose in neurodegeneration is important (42).
When your body is no longer utilizing insulin efficiently to make use of glucose in your cells, you are insulin-resistant.
When the resistant cells are the receptors in your brain that allow insulin to cross the blood-brain barrier, your brain begins to feel the effects.
Your brain cells require a lot of energy, which they get from glucose.
But they also need insulin to process that glucose, and if enough insulin is not getting to those cells, memory, cognition, and other functions start to suffer.
Insulin is also partially responsible for moving beta-amyloid proteins through your brain, and so a lack of it will disrupt synapses.
Prolonged insulin resistance, therefore, can lead to Alzheimer’s disease (43).
Prolonged or profound stress is a risk factor for Alzheimer’s.
When we are under stress, our bodies produce corticotropin-releasing hormone (CRH) in our stress hormone system, known as the hypothalamic–pituitary–adrenal (HPA) axis (44).
CRH is made by your body to help you respond to times of stress in different ways.
This hormone is responsible for the release of cortisol, as well as for suppressing appetite, increasing anxiety, improving selective attention for a short time, and triggering inflammation in various parts of the body.
As we age, our HPA axis changes which affects the production of stress hormones.
These changes can lead to increased risk of Alzheimer’s disease.
Elevated levels of CRH can stimulate beta-amyloid plaque formation, raising the risk of Alzheimer’s development (45).
Even post-traumatic stress disorder can increase beta-amyloid levels, which raises CRH during stress response (46).
Researchers studying Alzheimer’s changes in the brains of stressed mice noted they were more affected by chronic social stress, showed acceleration of beta-amyloid plaque buildup, and had a higher incidence of signal disruption to the brain.
These animals exhibited increased levels of beta-amyloid inside the nerves, showed signs of increased anxiety, and had other neurological changes (47).
Once a patient develops Alzheimer’s the CRH levels significantly decrease in the brain, which impacts the production of acetylcholine, a neurotransmitter that helps with memory and learning.
Researchers are unclear at this time on the effects of increasing CRH levels in mild-to-moderate Alzheimer’s patients, but this therapy could hold promise some day for slowing the disease’s progression.
Aluminum is an element that is toxic to nerve cells and could be a cause of Alzheimer’s.
Drinking water polluted with too much aluminum has been correlated with a higher incidence of Alzheimer’s disease (49).
As we age, testosterone levels decrease in both men and women.
When this happens, the risk of Alzheimer’s disease increases (52).
Testosterone is linked to the amyloid precursor (APP), which has neuroprotective properties, and elevating testosterone levels has been shown to decrease beta-amyloid levels in neurons.
Raising testosterone levels in elderly men may provide some protection against Alzheimer’s by raising APP.
Meta-analysis of 240 cases of elderly men was examined from over 5000 samples, and the data support the hypothesis that low testosterone levels are significantly associated with increased risk for Alzheimer’s disease (53).
How is Genetics Linked to Alzheimer’s?
It is undeniable that genetics play a role in the development of Alzheimer’s disease, but not all genes are created equally.
Two different types of genes, risk and deterministic, can contribute to your risk of developing Alzheimer’s, so it is therefore important that you understand both.
Risk genes do not guarantee you will develop a disease but do increase the likelihood you will do so in your lifetime.
There are several known risk genes associated with Alzheimer’s.
When you inherit risk genes from one parent, your risk rises, and when you inherit risk genes from both parents, your risk rises even more.
If you are a carrier of more than one copy of the EPOE-e4 gene, you could develop the disease at an earlier age, as well (56).
The Apolipoprotein E (APOE) gene’s significance is due to its primary function as a transporter of cholesterol and a repairer of injuries in the brain (57).
This gene is partially responsible for beta-amyloid protein digestion in neurons, so when it malfunctions, it has implications for Alzheimer’s.
Your body produces copies of this gene for various reasons, but those copies are not always identical to the original.
When the gene mutates to the APOE-ε2 copy, you are actually very unlikely to develop Alzheimer’s, as it is a strong neuroprotector (58).
The APOE-e4 gene is one of several forms of the APOE gene, and while researchers are still trying to understand how the gene increases risk, it not only raises the risk of having Alzheimer’s disease, but those with the gene are also more likely to develop the disease earlier in life.
Other genes that support the proper use of beta-amyloid proteins in the brain include the PSEN1 gene.
A mutation in this gene increases your risk of developing Alzheimer’s earlier, or of developing more aggressive forms of the disease.
This gene contributes to severe loss of neurons, plaque formation, and NFT (59).
Deterministic genes mean you will develop a disease if you inherit the gene.
One type of Alzheimer’s, known as familial Alzheimer’s, is caused by deterministic variations to the genetic code of the Presenilin gene.
This type of Alzheimer’s is a rarer form of the disease than others, afflicting less than one percent of those with Alzheimer’s.
Talk to your doctor about a genetic test if someone in your family has familial Alzheimer’s, or if you have several family members who have developed Alzheimer’s (60).
Other Genetic Links
There are other genetic markers that have been noted in patients with Alzheimer’s, but the extent to which these are responsible for the disease or serve as risk factors are not fully understood at this time.
The Nitric Oxide Synthase 2 (NOS2) gene helps deliver nitric oxide to your neurons, and Alzheimer’s patients often have high, toxic levels of nitric oxide (61).
When cells are past their usefulness and need to be removed from the body, they are programmed for cell death, also called apoptosis.
The Caspase 3 (CASP3) gene is involved in apoptosis, and it has been considered a possible trigger for the neurodegeneration of Alzheimer’s disease (62).
Finally, those with certain genetic structures are more susceptible to environmental influences, such as pesticides and other pollutants.
At this time, researchers are examining the link between pesticides, the GSTP1 gene, and the CYP2D6 gene to determine their risk factors for Alzheimer’s disease (63).
How Can I Prevent Alzheimer’s?
While there is no cure for Alzheimer’s disease, it is possible to reduce your risk and possibly prevent Alzheimer’s from developing.
Researchers continue to share new advancements in Alzheimer’s treatment, but following these guidelines can help you reduce your risk of developing dementia and other neurodegenerative disorders.
The best offense is a good defense, and this is true in matters of your health and well-being, as well as other parts of life.
Knowing both your predetermined risks, as well as those from your lifestyle that you can control, will be important for helping you be aware of how Alzheimer’s could affect you as you age.
Get an Education
When you participate in formal education, your brain builds a complex system of neural pathways, known as your cognitive reserve (64).
If you have many risk factors for Alzheimer’s, a good defense is to build up your cognitive reserve with education, study, and learning.
This allows your brain to develop alternative pathways for communication and association, which can assist you if you develop Alzheimer’s later in life (65).
As the disease shuts down neurons and neural pathways, your cognitive reserve can allow you to adjust and continue living with little to no disruption.
Increase Your Social and Mental Activity
If Alzheimer’s disease runs in your family, it is especially important that you maintain social relationships and engage in stimulating cognitive activities throughout your life and into old age.
By keeping your brain engaged and working on new tasks and learning, you create a more cognitive reserve, stimulate neural pathways so they do not degenerate, and help reduce your risk of Alzheimer’s disease (66).
As with all aspects of your health, eating right and getting exercise are always smart choices.
Exercise delays neurodegeneration improves memory, enhances cardiovascular health, and provides protection against cognitive impairment and Alzheimer’s disease (67).
Avoid a Fully-Western Lifestyle
As previously noted, Alzheimer’s is a modern-day disease, rising in incidence with the introduction of the modern diet and lifestyle (68).
Prior to recent decades, the rate of Alzheimer’s diagnosis was relatively steady, but it has risen sharply in recent years.
The areas of the world with the lowest incidence of Alzheimer’s are third-world countries in Africa, India, and South Asia (69).
While this may indicate genetic factors that contribute to the risk of Alzheimer’s, it is also clear that, when people adopt Western diets and lifestyles, the rate of Alzheimer’s increases significantly for that population (70).
As entire cultures, like the Japanese, shift toward Western habits, their incidence of dementia is rising sharply (71).
Eat a Mediterranean Diet
The diets of countries along the Mediterranean Sea are high in fresh fruits and vegetables, healthy fats, and seafood.
The Mediterranean diet reduces inflammation, reduces blood clots, and promotes brain health (74).
When Should I See a Doctor?
While it can be difficult to differentiate the signs of normal aging from those of Alzheimer’s disease and other dementia disorders, it is important to remember that the severity and frequency of these behaviors are key.
Consult your doctor when you notice that you or someone you love is experiencing one or more of these symptoms with regularity, or if the symptom is worsening over time (75).
Talk to your doctor if you:
- Often forget things or struggle to retain what you have just learned.
- Forget how to do something you have done for years.
- Frequently forget words, or use words that don’t fit the context.
- Forget often the day of the week.
- Get lost in familiar places.
- Have trouble recognizing a medical problem.
- Wear clothing very inappropriate for the weather.
- Have trouble with math or numbers.
- Put things away in unusual places.
- Have severe mood swings.
- Sometimes feel paranoid or threatened.
- Have lost interest in spending time with others, or in doing things you love.
If you are concerned about any of these behaviors, talk to your doctor.
He or she can help you determine next steps and treatment options.
What are Pharmaceutical Treatments?
Alzheimer’s is a disease without a cure, and current pharmaceutical treatments are designed to target the symptoms of the disease rather than the underlying causes.
Because there is likely no one cause for this disease, a true cure for Alzheimer’s may never be discovered.
Researchers are continuing to examine both beta-amyloid and tau protein therapies as possible curative treatments for Alzheimer’s.
Alzheimer’s medications are primarily designed to improve patients’ quality of life (76).
Once more is known about the underlying causes of the disease and how these interact with individuals, drugs that can cure Alzheimer’s may become known.
The following are pharmaceuticals used to treat the symptoms of Alzheimer’s, with some degree of success.
As noted previously, glutamate is an excitatory neurotransmitter that is present in almost all parts of the brain.
When glutamate is overactive, it inflicts stress on neurons, including those responsible for memory and cognition.
Toxic levels of stress mean neurons cannot perform appropriately or may degrade (77).
In the Alzheimer’s brain, memantine has been shown to block the NMDA receptors, protecting them from the overexcitement of toxic levels of glutamate.
This drug slows the neurodegeneration caused by Alzheimer’s disease, (78) and holds the possibility for preserving brain function longer in Alzheimer’s patients.
As with glutamate, acetylcholine is another important neurotransmitter.
When acetylcholine levels are too low, brain function starts to break down, causing problems with memory and learning.
Cholinesterase inhibitors (ChEI) increase acetylcholine levels in the brain by blocking their normal breakdown.
This helps to compensate for neurodegeneration and the loss of healthy neurons in Alzheimer’s patients (79).
A 2002 study of 207 patients using double-blind trials confirmed results for donepezil, one type of cholinesterase inhibitor used in Alzheimer’s treatment.
Subjects taking ChEI have noted improved activity level, improved mental capacity, and feeling more positive overall (80).
These are important results for those dealing with the effects of Alzheimer’s disease.
Treatments for Behaviors Associated with Alzheimer’s Disease
Because current pharmaceutical treatments are focused on the symptoms of Alzheimer’s disease, it is important to note that many Alzheimer’s patients take medications to control or manage their behavior.
As the progression of the disease makes people more impulsive and more likely to suffer from mental health issues, intervening to keep patients safe and improve their quality of life may be necessary.
As the brain cells deteriorate, medication and other therapies may be needed to control irritability, anxiety, depression, sleep disorders, hallucinations, delusions, and other behavioral manifestations of Alzheimer’s.
Beyond medication, there are many behavioral interventions and environmental modifications that can support the quality of life for those with Alzheimer’s disease.
When behavioral changes are noticed by caregivers, it is important to determine any triggering events, to consider the safety and well-being of the patient, and to evaluate medication side effects and interactions.
Because difficulty communicating is common in moderate-to-severe Alzheimer’s patients, determining the reasons for changes to behavior may be difficult, so considering a wide variety of reasons for behavior changes is necessary.
If behavioral and environmental approaches to behavior management have been tried and proven unsuccessful, medications may be necessary to alleviate severe symptoms in some Alzheimer’s patients.
The use of drugs in dementia patients is often unpredictable, so any drug therapies should be used under the careful supervision of a qualified physician.
Other Conventional Treatments
Some treatments and therapeutic measures for dealing with the symptoms of Alzheimer’s have been tested in small samples or using animal trials, but have not shown clinical performance in humans.
These therapies could offer options for Alzheimer’s patients in the future and should be watched carefully as research develops on their use.
Methylene blue has been studied as a prophylactic and treatment for Alzheimer’s disease.
By attenuating the accumulation of beta-amyloid plaque and NFT, methylene blue may hold promise for future research.
Because methylene blue also influences other Alzheimer’s hallmarks, including acetylcholine and glutamate, it could be an effective Alzheimer’s treatment (81).
It works by slowing the rate at which normal human cells age, which could delay the onset of Alzheimer’s in those with risk factors (82).
Current animal trials show methylene blue to be effective at reducing beta-amyloid levels, leading to slower cognitive decline (83).
Sirtuins, Polyphenols, and NF-κB
Treatments that protect against the aging process could have benefits for those suffering from diseases like Alzheimer’s and dementia.
Sirtuins such as SIRT1 show promise in mouse models for slowing beta-amyloid deposits.
Dietary polyphenols can mitigate some of the damage done to cells as part of the aging process, too.
They work by increasing SIRT1 activity.
Targeting specific proteins in our cells that mediate the aging process represents a possible Alzheimer’s treatment.
By inhibiting NF-κB in cells, we can delay the start of age-related issues and diseases (87), such as Alzheimer’s.
Focusing on how to inhibit these proteins holds promise for future research in this field.
The Future of Alzheimer’s Drug Research
Researchers have made great strides in understanding brain function and Alzheimer’s dysfunction over the past 30 years.
The next generation of Alzheimer’s treatments will focus primarily on three main areas: beta-amyloid plaque reduction, promotion of healthy tau protein formation, and reduction of neural inflammation.
With a renewed focus on these three areas and advancements in technology that allow for targeted treatments to specific enzymes and compounds, future drug therapies for the treatment and prevention of Alzheimer’s will likely come from a combination of these areas of research.
Natural Treatments for Alzheimer’s Disease
While pharmaceuticals and other conventional medical treatments report limited success in treating Alzheimer’s symptoms, there are other, natural therapies that produce effective results as well.
These treatments are good for staving off Alzheimer’s longer, and for promoting a healthy life that prevents the onset of dementia and other brain disorders.
As the healthy heart/healthy brain connection is still being studied, our understanding of the impact of exercise on brain health is developing.
Increased physical activity has been shown to reduce plaque buildup in the brains of mice (88).
Alzheimer’s patients who walk regularly show improved performance in activities, and have a reduced incidence of other mental health issues like depression (89).
Those who have Alzheimer’s disease are often at risk for falling, so staying active and strong can improve balance and mobility.
Using resistance training as well as promoting cardiovascular health will assist you as you age in staying strong and healthy (90).
Exercising your brain is just as important as your muscles.
Mental activity that is moderate can reduce the effects of Alzheimer’s in midlife and beyond, and those with active minds are less likely to develop Alzheimer’s disease (91).
Cognitive activity builds neural connections, maintains the health of your brain tissue, and increases brain volume, all of which help stave off dementia and other brain disorders.
Mental activities such as playing games, solving puzzles, and reading can help you stay sharp as you age (92).
Activities that require memory, problem-solving, and learning new tasks increase your cognitive load and provide a good workout for your brain (93).
While more research is needed in this area, there is little doubt that using your brain in challenging ways has positive benefits for lowering the risk of Alzheimer’s.
Research suggests that Vitamin E can slow neurodeterioration in patients with moderate-to-severe Alzheimer’s disease (94).
Alzheimer’s causes oxidative damage, so using antioxidant therapy such as Vitamin E has potential as a treatment for the disease (95).
While this type of treatment is still new, the use of Vitamin E shows promise because it crosses the blood-brain barrier more easily, compared to other antioxidants like Vitamin C and beta-carotene (96).
Additional research is needed in this area to determine the overall implications of Vitamin E for patients with Alzheimer’s disease.
Vitamin D and Sun Exposure
Your body manufactures Vitamin D when your skin is exposed to sunlight.
While Vitamin D works with calcium to build strong bones, it also helps regulate the immune system and is important to the life cycle of human cells, including brain cells.
Many patients with Alzheimer’s and other dementia diseases are Vitamin D-deficient.
Alzheimer’s patients often do not get enough sun exposure, resulting in low levels of this important vitamin (99).
When those with Alzheimer’s do not see enough sunlight, it not only impacts Vitamin D levels but disrupts sleep quality, which also contributes to Alzheimer’s development (100).
When you don’t get enough sun, your circadian rhythms, or how well you experience day versus night and when you naturally feel tired, are disrupted.
If patients cannot safely go outside for natural sunlight, using near-infrared light therapy can have health benefits (101).
This type of light can slow or even stop neurodegeneration, so this treatment continues to be researched for patients with Alzheimer’s.
Increased exposure to natural light or near-infrared light promotes healthier sleep, particularly in patients with severe Alzheimer’s disease (102).
When combined with melatonin, light therapy can boost mood and improve symptoms for Alzheimer’s sufferers (103).
In addition to helping promote better sleep, melatonin has many benefits for those with Alzheimer’s disease.
Alzheimer’s patients often have lower functioning in the melatonin receptors MT1 and MT2 (106).
Low levels of this important compound definitely contribute to sleep disruption, which raises the risk for Alzheimer’s, and impacts symptoms.
Melatonin has been shown to lessen Alzheimer’s symptoms, as well as prevent certain types of neuron cell death in laboratory animals.
Manganese and Potassium
While there is no causal evidence that manganese deficiency causes Alzheimer’s, we do know that most patients with Alzheimer’s have low levels of manganese in their blood, making manganese deficiency a risk factor for the disease (109).
When you are deficient in manganese, your body can experience mitochondrial dysfunction, and levels of glutamate can rise in the brain (110).
Both of these are symptoms seen in most Alzheimer’s patients, so further research is needed to understand this link.
Without proper levels of potassium in our systems, our bodies cannot process beta-amyloid correctly, and we see rises in oxidative stress and inflammation.
Increasing potassium intake can improve cognitive performance, as well as help, prevent the onset of Alzheimer’s disease (111).
Plants have many restorative and curative properties, and there are some herbs that can promote the necessary brain processes to help prevent Alzheimer’s disease.
Saffron and turmeric both have been observed to have beneficial results for those with Alzheimer’s, and offer promise with further research and understanding.
The use of saffron as a safe and effective treatment for mild-to-moderate Alzheimer’s disease has been studied in several scenarios.
Fifty-four subjects in a 22-week double-blind study took saffron or donepezil, and cognitive measures determined no significant difference between treatments.
Saffron also has antioxidant properties which reduce neurodegeneration and protect against damage by free radicals (114).
Another herb with promise for Alzheimer’s prevention and treatment is turmeric, which contains a compound known as curcumin.
Because of its properties as an anti-inflammatory and antioxidant, curcumin can improve cognitive function by lowering beta-amyloid plaque formation.
Neurodegradation is slowed, and memory improves when Alzheimer’s patients are given curcumin (115).
In addition to curcumin, turmeric also contains demethoxycurcumin and bisdemethoxycurcumin.
These curcuminoids work together efficiently to produce better results and are more effective than pure curcumin alone.
Curcumin and the other curcuminoids have positive effects, not only on the beta-amyloid plaque, but also tau proteins, acetylcholine levels, and insulin resistance in the brain, all of which influence the development of Alzheimer’s disease (116, 117).
Further research is still needed to determine curcumin’s full potential in the treatment of Alzheimer’s, but this herb offers many possibilities that should be examined further.
In addition to using sugar as a fuel source, the brain can also effectively use fats, which the body breaks down into ketone bodies, for energy in the brain.
Ketosis is the metabolic process of using stored fats for energy, and it is a normal function of your body.
When you supply your body with appropriate ketones, such as medium-chain triglycerides like those in coconut oil, there can be improved memory function for Alzheimer’s patients (118).
In order to promote ketosis, you can use intermittent fasting to encourage your body to use fats instead of glucose, and you can consume a ketogenic diet which is low in carbohydrates (119).
When in ketosis, your body creates less oxidative stress and damage to neurons, while also supplying the brain with more efficient mitochondrial energy.
This process reduces glutamate levels and promotes healthier brain function (120).
As discussed previously, eating a Mediterranean diet that includes olive oil has beneficial results for Alzheimer’s patients.
In animal tests, olive oil promoted improved memory and significant new cell growth.
Huperzine A is derived from Chinese club moss, and while this drug does come from a natural substance, it is highly purified and manipulated in a lab to create the substance used to treat Alzheimer’s.
Recent studies have examined the effectiveness of Huperzine A in the treatment of Alzheimer’s disease for its ability to decrease the rate of cognitive decline (123).
By halting apoptosis, or cell death, Huperzine A lowers inflammatory response in neurons (124).
Its anti-inflammatory properties should be examined more closely for potential benefits in Alzheimer’s disease treatment.
MitoQ and Phosphatidylserine
When your cells break carbohydrates and fats down to release their energy, oxidative damage naturally occurs.
Excess oxidative damage is often seen in Alzheimer’s patients, so mitigating this damage is important.
MitoQ is a mitochondria-targeted antioxidant that has promise for preventing the buildup of beta-amyloid proteins, neuronal loss, and cognitive decline associated with Alzheimer’s disease (127).
Some even note improved spatial memory using MitoQ (128).
By protecting the mitochondria and allowing them to work more efficiently, other neural functions are preserved, extending lifespan in some animal tests (129).
Phosphatidylserine is a chemical your body can make naturally, but we also get most of it we need from food.
It is part of the structure of all of your body’s cells and is important for maintaining cellular function.
This is especially true in your brain, where phosphatidylserine promotes mental function by preventing beta-amyloid accumulation (130).
It also improves the metabolism of glucose in the brain, which is linked to Alzheimer’s.
When you have appropriate levels of phosphatidylserine, you can prevent Alzheimer’s, or slow the disease’s progression (131).
Taking a phosphatidylserine supplement could have positive effects for those with Alzheimer’s risk factors.
Other Potential Natural Treatments
There may be other natural compounds and processes that can protect against or reduce the risk of Alzheimer’s disease.
As new treatments are being studied all the time, we are learning more about innovative ways to tackle this illness.
The following are natural treatments that hold promise for future research and possible therapeutic benefits in helping Alzheimer’s patients.
- Gotu Kola is an herbaceous plant native to Asia. In test-tube models, Gotu Kola was successful at preventing neuronal death by mitigating the impact of beta-amyloid (132).
- Low-level laser therapy, or LLLT, has been used in animal trials successfully to improve spatial reasoning and cognitive capacity by degrading beta-amyloid (133).
- Lithium has been tested in Alzheimer’s animal models and has been shown to provide neuroprotection and improve cognitive functioning (134).
- Phytic acid could provide some protection against neuron cell damage and amyloid toxicity inside the brain (135).
- Caffeine has some neuroprotective properties that could be used to treat dementia and other diseases associated with aging (136).
- THC and CBD, both derived from cannabis, can inhibit beta-amyloid plaque formation (137). THC also lowers rates of cell death and decreases inflammation, while CBD has successfully reversed deficits to cognition in mice (138, 139, 140, 141).
- Sodium benzoate may be effective in the early stages of Alzheimer’s development for improving cognition and overall brain function (142).
- Resveratrol is a polyphenol with neuroprotective properties. This antioxidant has been tested in animal models as a possible Alzheimer’s treatment (143).
- Apigenin may be able to slow the onset of Alzheimer’s disease through neuroprotective and anti-inflammatory properties. Apigenin is also an antioxidant, and prevents beta-amyloid plaque, giving it real promise as an Alzheimer’s treatment (144).
- Hesperidin has been successful in mouse models for improving cognition and reversing mitochondrial dysfunction (145).
Because Alzheimer’s disease continues to grow in prevalence and little is still known definitively about its underlying causes, medical research continues to study this degenerative disorder.
As the number of those afflicted with Alzheimer’s grows, we can hope that our understanding of how to treat, and someday prevent, this disease of aging effectively will grow as well.
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