Skip to main content

8 Signs of Toxic Alzheimer’s Disease

Younger Onset

Occurs at a younger age than other subtypes, often 45-60 years old.


Difficulty with math, organization, words, spelling, and reading.

Trouble With Simple Tasks

You may sometimes forget how to complete everyday tasks.

Frequent Misdiagnosis

Symptoms often misdiagnosed as ADD or depression.

Elevated Inflammatory Markers

High levels of CRP, IL -6, and TNF seen in labs.

High Toxin Levels

Multiple toxins testing at above normal levels.

No Family History

Minimal or no family history of AD.

Increased Genetic Risk

ApoE3 and HLA-DR/DQ genes are associated with toxic AD.

Subtype No. 3


Alzheimer’s Disease

The toxic subtype of Alzheimer’s disease (AD) is dramatically different from the other subtypes. The underlying causes of toxic Alzheimer’s are unique, as well as the type and timing of symptoms.



Training on Toxins

Medical schools and residency training programs teach about the acute effects of being exposed to large doses of toxins. For example, toxic levels of exposure to things like mustard gas, street drugs, prescription drugs, coal factory fumes, lead, and other heavy metals.

However, the idea that small amounts of heavy metals, everyday environmental chemicals, pesticides and herbicides, flame retardants, mold, pollution, and plastics can build up in our bodies over time and result in complex chronic diseases like AD and other dementias remains poorly understood in the conventional medicine realm.

The research on the relationship between many of these “everyday” toxins and AD is growing rapidly and has reached the point where it absolutely cannot be ignored. (1)


Toxins and

Cognitive Health

Toxins can have a large impact on brain health and performance because toxins are fat-soluble. This means that they don’t dissolve in water, so your body can’t eliminate them very well via two of your primary elimination pathways: urine and stool. For this reason, toxins in your body tend to accumulate in fatty tissues.

Guess what your brain is primarily made of?

You guessed it, fat. Your brain is basically a toxin magnet.


How Does Toxin

Exposure Occur?

Toxin exposure can come through things that you eat, drink, breathe, and touch. The list of chemicals an individual is exposed to daily has grown exponentially over the past 50 years and can be found in food, water, air, clothes, sheets, car, and the personal care products you put on your skin, hair, and nails, among other things.

“We are constantly and increasingly exposed to a variety of toxins that can have profound effects on our brain health. Taking steps now to minimize toxins in your immediate environment and improving your body’s natural detoxification processes can help mitigate damage and prevent toxin-related cognitive decline.”

Dr. Scott Noorda, DO

Family Physician, Precision Medicine

Signs + Symptoms


This subtype often occurs at a younger age, with symptoms typically starting in the late forties to the early sixties. Frequently symptoms initially manifest or are significantly exacerbated following major stress.

The initial symptoms with the toxic subtype are usually not the same as with other subtypes of AD. For example, most other types of dementia start with symptoms of amnesia or memory loss. However, toxins seem to first produce other symptoms, such as problems with math, organization, speaking (particularly with word-finding), spelling, and reading.

As memory loss occurs it doesn’t follow the typical pattern. Instead of losing recent memory first with a progressive loss of older (remote) memories over time, these patients lose both old and new memories. They also start to forget how to do things they used to know how to do, sometimes even simple things.

Additionally, these patients can initially be misdiagnosed with other conditions such as ADD, depression, frontotemporal dementia, or atypical dementia because of the above-mentioned symptoms in addition to associated difficulty concentrating and depressed mood. (13)

Genetic Factors


A question we’re routinely asked is, why would two people exposed to similar toxins throughout their lives don’t both develop AD and other chronic diseases? The answer is complex, but basically, the difference lies in the interaction of how their genetics, environment, and lifestyle influence their body’s ability to effectively eliminate toxins.

Interestingly, the toxic subtype of AD is more often seen in people who carry the ApoE3 (low risk) gene, rather than the ApoE4 gene (classically tied to AD). Thus, these people usually don’t have a strong family history of AD.

Certain types of the HLA-DR/DQ genes are associated with multiple sensitivities to mycotoxins from mold or toxins from other microbes, and thus can increase your risk of not eliminating these toxins and having more detrimental effects on the brain. (13)

Lab Indications


Different subtypes can’t always easily be distinguished by lab testing, but there are some unique findings in the toxic subtype that are worth mentioning.

Levels of heavy metals, mold, and environmental toxins can be assessed directly with urine (most accurate) and hair testing.

Lab findings in AD caused by toxins include any of the following:

  • Low triglycerides (<60mg/dL)
  • Low zinc (<75mcg/dL) and/or a high copper to zinc ratio (>1.3)
  • Hormonal abnormalities
    • Abnormal ACTH levels (brain signal to the adrenal gland)
    • Low pregnenolone
    • Low DHEA-S (sulfate)
    • Low morning cortisol

Target levels for these nutrients and hormones aren’t always the levels shown as normal by different lab companies. Discuss them with a practitioner trained in optimizing and personalizing these lab findings.

MRIs don’t only show the typical brain atrophy in memory areas like the hippocampus, but the atrophy can be much more widespread. Multiple abnormal spots are also often seen in the white matter, resulting from greater neuroinflammation and leakiness of blood vessels. (13)

Alzheimer’s Prevention Articles

1. Genuis, S. J., & Kelln, K. L. (2015). Toxicant exposure and bioaccumulation: a common and potentially reversible cause of cognitive dysfunction and dementia. Behavioural Neurology, 2015.
2. Sobel, E., & Davanipour, Z. (1996). Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer’s disease. Neurology, 47(6), 1594-1600.
3. Wu, S., Liu, H., Zhao, H., Wang, X., Chen, J., Xia, D., … & He, Y. (2020). Environmental lead exposure aggravates the progression of Alzheimer’s disease in mice by targeting on blood brain barrier. Toxicology letters, 319, 138-147.
4. Niño, S. A., Morales-Martínez, A., Chi-Ahumada, E., Carrizales, L., Salgado-Delgado, R., Pérez-Severiano, F., … & Zarazúa, S. (2018). Arsenic exposure contributes to the bioenergetic damage in an Alzheimer’s disease model. ACS chemical neuroscience, 10(1), 323-336.
5. Mutter, J., Naumann, J., Schneider, R., & Walach, H. (2007). Mercury and Alzheimer’s disease. Fortschritte der Neurologie-psychiatrie, 75(9), 528-538.
6. Tang, B. L. (2020). Neuropathological Mechanisms Associated with Pesticides in Alzheimer’s Disease. Toxics, 8(2), 21.
7. Cattani, D., Cavalli, V. L. D. L. O., Rieg, C. E. H., Domingues, J. T., Dal-Cim, T., Tasca, C. I., … & Zamoner, A. (2014). Mechanisms underlying the neurotoxicity induced by glyphosate-based herbicide in immature rat hippocampus: involvement of glutamate excitotoxicity. Toxicology, 320, 34-45.
8. Bredesen, D. E. (2016). Inhalational Alzheimer’s disease: an unrecognized—and treatable—epidemic. Aging (Albany NY), 8(2), 304.
9. Lagergren, M., Fratiglioni, L., Hallberg, I. R., Berglund, J., Elmståhl, S., Hagberg, B., … & Wiberg, I. (2004). A longitudinal study integrating population, care and social services data. The Swedish National study on Aging and Care (SNAC). Aging clinical and experimental research, 16(2), 158-168.
10. Yegambaram, M., Manivannan, B., G Beach, T., & U Halden, R. (2015). Role of environmental contaminants in the etiology of Alzheimer’s disease: a review. Current Alzheimer Research, 12(2), 116-146.
11. Agarwal, P., Brockman, J. D., Wang, Y., Schneider, J. A., & Morris, M. C. (2020). Brain Bromine Levels Associated with Alzheimer’s Disease Neuropathology. Journal of Alzheimer’s Disease, (Preprint), 1-6.
12. Sobel, E., & Davanipour, Z. (1996). Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer’s disease. Neurology, 47(6), 1594-1600.
13. Bredesen, D. (2017). The End of Alzheimer’s: The first program to prevent and reverse cognitive decline. Penguin. pp. 104-108.