Causes of Alzheimer’s Disease
Alzheimer's disease is a devastating diagnosis for both the patient and their family members. With new research, however, comes new hope for treatment, prevention and even reversal of the disease.
Although early-onset Alzheimer’s occurs, most cases are in those over age 60. In fact, Alzheimer’s disease is the fifth leading cause of death for those over age 65. In 2020, Alzheimer’s affected up to 5.8 million Americans and this is projected to triple, reaching 14 million diagnoses by the year 2060. (Source 1)
If Alzheimer’s disease has affected you or someone you know, which is likely the case given these statistics, then this article is for you.
Keep reading to learn more about:
- What is Alzheimer’s disease
- How functional medicine views Alzheimer’s differently
- New research identifying risk factors
- New research in the areas of diagnosis and treatment strategies
- Lifestyle pieces to consider for prevention
Let’s get started!
What Is Alzheimer’s Disease?
Alzheimer’s disease is the most common form of dementia globally. It’s a progressive disease. In the early stages, a person may experience mild cognitive impairment and memory loss that show up as getting lost, losing objects or forgetfulness, as examples.
As the disease progresses, routine daily activities become increasingly difficult. Those with Alzheimer’s will eventually need care for daily life, often from family members or other caregivers.
Alzheimer’s disease is characterized by plaque build-up in the brain over time. A component of this plaque, known as beta-amyloid or amyloid beta, which are toxic proteins associated with the cognitive decline of Alzheimer’s disease.
Symptoms of Alzheimer’s disease may include:
- Memory loss
- Impairment of cognition and thinking
- Changes in language
- Changes in behavior
- Changes in judgement
- Withdrawal from social activities
- Changes in personality
Most Alzheimer’s patients also experience neuropsychiatric symptoms such as depression, aggression, apathy, delusions and psychosis. (Source 2)
A Functional Medicine Approach to Alzheimer’s
The conventional healthcare model is mainly focused on managing symptoms and delaying the progression of Alzheimer’s disease. In addition, several Alzheimer's-specific medications have not been that successful and side effects are common.
Functional medicine takes a different approach. We know that the disease process and changes in the brain begin prior to the onset of symptoms, which allows for the possibility of prevention and disease reversal, with early intervention.
In the treatment of Alzheimer’s disease, functional medicine considers each individual’s unique root causes. Because each person has many root causes, a singe intervention or medication may not work. Often, many interventions are needed at once.
Dr. Dale Bredesen is a doctor and researcher who has dedicated his career to studying Alzheimer’s disease. Through a functional medicine approach, he has shown the reversal of cognitive decline in Alzheimer’s disease using his framework and root cause approach. (Source 3)
Risk Factors and Root Causes of Alzheimer
Age is the number one risk factor for Alzheimer’s disease. Family history also plays a role.
When taking a root cause approach, we also consider:
- Nutrient deficiencies
- Inflammation
- Oxidative stress
- Toxin exposure and accumulation
- Insulin resistance
- Mitochondria disfunction
These root causes also play a role in the development of obesity, diabetes, high blood pressure, heart disease and other chronic conditions more likely to affect older people. Let’s look at some recent research uncovering additional root cause pieces to Alzheimer’s specifically.
Liver Health and Lipids
We know that amyloid plaques build up in the brain, affecting brain tissue and function. New research suggests that toxic proteins (beta amyloid) don’t originate in the brain; they may be produced in the liver and packaged into lipoproteins to be carried in the blood. (Source 4)
Just like we talk about leaky gut, the brain can also be leaky. When the blood brain barrier becomes more permeable, often due to inflammation, it may allow for the beta amyloid to be deposited in the brain. (Source 4)
In this mouse model study, the mice that produced lipoprotein-amyloid in the liver, had brain inflammation, brain cell death and memory loss. (Source 4)
This new understanding of the blood-to-brain pathway in Alzheimer’s may lead to new treatments that inhibit amyloid beta from getting into the brain.
APOE – Apolipoprotein E
Apolipoprotein E, or APOE, is the major cholesterol carrier in the brain, involved in neuronal growth and membrane repair. It is coded for by the gene APOE, of which three alleles are possible: ApoE2, ApoE3 and ApoE4. We all have two copies. (Source 5)
Having the ApoE4 allele is the strongest genetic risk factor for Alzheimer’s disease. ApoE4 doesn’t just promote mechanisms related to beta amyloid; it is also involved with neurofibrillary degeneration, microglia (a type of brain cell) response, disruption of the blood brain barrier, and changes in nerve cells, all of which contribute to cognitive impairment. (Source 6)
About 25 percent of Americans are APOE4 carriers, which increases risk of Alzheimer’s fourfold if one copy is present and 14-fold if to copies present compared to ApoE3. ApoE4 is also involved in neurological disorders, other types of dementia and down syndrome. ApoE2 is considered neuroprotective. (Source 5)
As I’ve talked about in previous articles, our genes are not our destiny. We can modify what genes are expressed through diet and lifestyle. For example B vitamins support methylation and vitamin C is important for demethylation (add link to recent vitamin C article) at the genetic level.
Vitamin B12
Low blood levels of folate and vitamin B12, along with elevated homocysteine levels are risk factors for dementia, reduced cognitive function and Alzheimer’s disease. (Source 7) These nutrients are all a part of the methylation cycle.
A recent worm study reveals more about the importance of vitamin B12. Researchers found that worms don’t wiggle when they have Alzheimer’s. Why? Turns out that beta amyloid paralyzes worms.
When worms were fed E. coli with a higher amount of vitamin B12, they didn’t develop Alzheimer’s and continued to wiggle, despite the same amounts of amyloid beta as seen in the worms deficient in vitamin B12. This suggests a protective effect of vitamin B12. (Source 8)
Advances in Testing and Treatment of Alzheimer’s
Understanding mechanisms and underlying causes is only one area of current Alzheimer’s disease research. We are also learning more about early detection and treatment possibilities all the time.
A new PET scan, called amyloid positron emission tomography, or amyloid PET for short, is being used to estimate when a high-risk person will develop Alzheimer’s disease. Since amyloid beta silently builds up for years and even decades before cognitive changes are seen, this calculation, based on the brain scan results, the person’s age and ApoE4 status helps to estimate the tipping point where memory problemsappear. (Source 9)
Eventually, we may have a blood marker for Alzheimer’s disease as well. A pilot study compared blood of those with Alzheimer’s disease to healthy controls. Those with Alzheimer’s had protein accumulation on red blood cells themselves, that included beta amyloid peptides and tau proteins. These fibers were much greater than the controls. This information may pave the way for an easy screening tool to assess the stages of Alzheimer’s. (Source 10)
On the treatment front, scientists are exploring a new antibody structure that allows for better binding to the amyloid beta clumps called aggregates, which stops or stalls their harm to neurons. (Source 11)
In addition, chemotherapy might have a new application. When mice with Alzheimer’s disease were given Axitnib, a chemotherapy cancer treatment, it helped to restore memory and cognition. This therapy is interesting because unlike other Alzheimer’s medications, it doesn’t target amyloid beta. Instead, it targets the vascular system by decreasing the growth of abnormal blood vessels in the brain that are seen in both Alzheimer’s disease and brain tumors. Clinical trials are needed. (Source 12)
Alzheimer’s Prevention and Addressing Root Causes
Although much effort is put into detection and treatment, preventing Alzheimer’s disease in the first place and addressing root causes early in the disease process should be of top priority.
While you can’t change your age, or your genetics, there are many modifiable risk factors such as diet, physical activity, sleep, stress and others that do impact gene expression, metabolic health and reduce the risk for developing chronic disease. These factors explain why some people with ApoE4 never go on to develop Alzheimer’s.
In addition to these lifestyle pieces, supplements may provide additional and targeted support. Supplements to consider include:
- Active Vitamin B12 and Folate – Keep vitamin B12 levels optimized as B12 has been shown to be protective of dementia. Both vitamin B12 and folate also support healthy methylation for optimal gene expression. These nutrients can be taken alone or as part of a comprehensive multivitamin and mineral complex.
- Optimized Liposomal PC Complex – Phosphatidyl choline, or PC, is important for brain health. It provides a main building block for cell membranes and mitochondria, supports a healthy blood-brain barrier and is important for liver health, which is where amyloid beta originates. Read more about the benefits of PC here.
- Liposomal Glutathione – Glutathione is the body’s master antioxidant that supports detoxification, protects the brain from oxidative stress and lowers inflammation. Unfortunately, glutathione levels decline with age. Lower levels of glutathione are also found in those with Alzheimer’s disease. (Source 13, 14)
- Liposomal Curcumin – Curcumin, the anti-inflammatory active compound in turmeric spice is used in both the prevention and treatment of Alzheimer’s disease. Besides reducing neuroinflammation, it has been shown to suppress beta-amyloid. (Source 15)
CoreMed Science’s liposomal supplements offer superior absorbability and bioavailability of key therapeutic nutrients. The liposomal delivery system mimics the structure of our own cell membranes, including brain cell membranes and mitochondria. Check out our full line of products, including the ones mentioned here regarding their use in Alzheimer’s disease.
While the onset of Alzheimer's disease was once thought of as a devastating death sentence, new research is coming out every day that points to earlier detection and new treatment options. I always recommend working with a functional medicine doctor, and in this case one that specializes in dementia or has been trained by Dr. Dale Bredesen would be ideal. Identifying the root cause pieces and working to address them with all the tools we have, including medicine, nutrition, lifestyle and supplements may just change or save your life.
References
1.Centers for Disease Control and Prevention. Alzheimer’s disease and healthy aging: Alzheimer’s disease and related dementias. Retreived October 20, 2021 from: https://www.cdc.gov/aging/aginginfo/alzheimers.htm#AlzheimersDisease
2.Lyketsos, C. G., Carrillo, M. C., Ryan, J. M., Khachaturian, A. S., Trzepacz, P., Amatniek, J., Cedarbaum, J., Brashear, R., & Miller, D. S. (2011). Neuropsychiatric symptoms in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association,7(5), 532–539. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299979/
3.Bredesen, D. E., Amos, E. C., Canick, J., Ackerley, M., Raji, C., Fiala, M., & Ahdidan, J. (2016). Reversal of cognitive decline in Alzheimer's disease.Aging,8(6), 1250–1258. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4931830/
4.Lam, V., Takechi, R., Hackett, M. J., Francis, R., Bynevelt, M., Celliers, L. M., Nesbit, M., Mamsa, S., Arfuso, F., Das, S., Koentgen, F., Hagan, M., Codd, L., Richardson, K., O'Mara, B., Scharli, R. K., Morandeau, L., Gauntlett, J., Leatherday, C., Boucek, J., … Mamo, J. (2021). Synthesis of human amyloid restricted to liver results in an Alzheimer disease-like neurodegenerative phenotype.PLoS biology,19(9), e3001358. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8439475/
5.Lanfranco, M. F., Ng, C. A., & Rebeck, G. W. (2020). ApoE Lipidation as a Therapeutic Target in Alzheimer's Disease.International journal of molecular sciences,21(17), 6336. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503657/
6.Serrano-Pozo, A., Das, S., & Hyman, B. T. (2021). APOE and Alzheimer's disease: advances in genetics, pathophysiology, and therapeutic approaches.The Lancet. Neurology,20(1), 68–80. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8096522/
7.Ma, F., Wu, T., Zhao, J., Ji, L., Song, A., Zhang, M., & Huang, G. (2017). Plasma Homocysteine and Serum Folate and Vitamin B12Levels in Mild Cognitive Impairment and Alzheimer's Disease: A Case-Control Study.Nutrients,9(7), 725. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537839/
8.Lam, A. B., Kervin, K., & Tanis, J. E. (2021). Vitamin B12impacts amyloid beta-induced proteotoxicity by regulating the methionine/S-adenosylmethionine cycle.Cell reports,36(13), 109753. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8522492/
9.Schindler, S., Li, Y., Buckles, V. D., Gordon, B. A., Benzinger, T., Wang, G., Coble, D., Klunk, W. E., Fagan, A. M., Holtzman, D., Bateman, R. J., Morris, J. C., & Xiong, C. (2021). Predicting Symptom Onset in Sporadic Alzheimer Disease With Amyloid PET.Neurology, 10.1212/WNL.0000000000012775. Advance online publication. Abstract:https://pubmed.ncbi.nlm.nih.gov/34504028/
10.Nirmalraj, P. N., Schneider, T., & Felbecker, A. (2021). Spatial organization of protein aggregates on red blood cells as physical biomarkers of Alzheimer's disease pathology.Science advances,7(39), eabj2137. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8462905/
11.Rofo, F., Buijs, J., Falk, R., Honek, K., Lannfelt, L., Lilja, A. M., Metzendorf, N. G., Gustavsson, T., Sehlin, D., Söderberg, L., & Hultqvist, G. (2021). Novel multivalent design of a monoclonal antibody improves binding strength to soluble aggregates of amyloid beta.Translational neurodegeneration,10(1), 38. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8477473/
12.Singh, C., Choi, K. B., Munro, L., Wang, H. Y., Pfeifer, C. G., & Jefferies, W. A. (2021). Reversing pathology in a preclinical model of Alzheimer's disease by hacking cerebrovascular neoangiogenesis with advanced cancer therapeutics.EBioMedicine,71, 103503. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8449085/
13.Liu, H., Wang, H., Shenvi, S., Hagen, T. M., & Liu, R. M. (2004). Glutathione metabolism during aging and in Alzheimer disease.Annals of the New York Academy of Sciences,1019, 346–349. Abstract: https://pubmed.ncbi.nlm.nih.gov/15247041/
14.Wu, G., Fang, Y. Z., Yang, S., Lupton, J. R., & Turner, N. D. (2004). Glutathione metabolism and its implications for health.The Journal of nutrition,134(3), 489–492. Abstract: https://pubmed.ncbi.nlm.nih.gov/14988435/
15.Chainoglou, E., & Hadjipavlou-Litina, D. (2020). Curcumin in Health and Diseases: Alzheimer's Disease and Curcumin Analogues, Derivatives, and Hybrids.International journal of molecular sciences,21(6), 1975. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139886/