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8 Signs of Traumatic Alzheimer’s Disease

Traumatic Brain Injury

A history of severe or multiple concussions.

Chronic Post-Concussion Symptoms

Problems with sleep, concentration, balance, coordination, and headaches.

Trouble Learning New Things

Difficulty learning new things and storing new memories and information.

Early Onset

Earlier onset than other subtypes, as early as 40’s or 50’s.

Elevated Inflammatory Markers

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

Leaky Gut

Antibodies to foods cross-reactive to amyloid-beta, like eggs, lentils, tuna, gluten, etc

Leaky Brain

Signs of blood-brain barrier permeability.

MRIs Show Trauma

Tiny bleeds, injury, softening, or loss of brain tissue.

Subtype No. 5


Alzheimer’s Disease

The traumatic subtype of Alzheimer’s disease (AD) has some unique features and very specific, identifiable underlying causes.

As the name suggests, this subtype of AD is caused by either major head trauma or recurrent smaller head and brain injuries whose effects accumulate over time.



Repetitive head trauma has been in the news a lot in the past 5-10 years because of the effects seen in famous athletes participating in sports like boxing, football, hockey, etc. The damage that occurs from multiple concussions has been shown to significantly increase one’s risk for AD (as well as for other conditions like depression, anxiety, ADHD, and Parkinson’s Disease). (1)

A concussion is a traumatic brain injury that negatively affects your brain function. Some concussions cause you to lose consciousness, but you can still have a concussion without loss of consciousness. Concussions are usually caused by a blow to the head and falls are the most common cause of concussions.

The risk of dementia increases with the number of TBIs [traumatic brain injuries] sustained. Even those who experience mild TBI are at increased risk of dementia compared with those who have not had a TBI.



Brain Injury

Concussions resulting in TBIs are common among those who serve in the military. One study looking at U.S. military veterans found that mild TBI is associated with a two-fold increase in the risk of being diagnosed with some type of dementia, including AD. (3)

Another study found that people with a history of TBI who develop Alzheimer’s do so at a younger age than those without a history of TBI. (4)

Interestingly, MRI images of the early stages of AD look very similar to MRI images of the brains of people who have suffered a traumatic brain injury (TBI). (5)

“The consequences of concussions are often underplayed as they have now become so common and the associated problems may not show up for several years. Optimizing brain health and neuroplasticity is key to avoiding and overcoming traumatic Alzheimer’s disease after multiple or severe traumatic brain injuries.”

Dr. Scott Noorda, DO

Family Physician, Precision Medicine

Signs + Symptoms


The symptoms for the traumatic subtype of AD typically start at a younger age compared with most other types of AD, with onset as early as one’s forties or fifties.

Most often the effects of concussions are temporary, but if there is significant trauma in the brain or they are repetitive, longer-lasting symptoms can occur, such as headaches, and difficulty with sleep, concentration, balance, and coordination. Symptoms of anxiety, irritability, anger, or depression can also occur. (6)

The memory loss most commonly associated with brain trauma is difficulty learning new things. This expands to more broad scope memory impairment as the disease progresses.

TBI can disrupt the intestinal barrier that normally functions to block the flow of certain minerals, nutrients, bacteria, and bacterial products between the inside and outside of the intestine. (7) This has been termed leaky gut. This can result in major inflammation throughout the body, creating symptoms of joint pains, brain fog, food, and chemical sensitivities, and even increase the risk for autoimmune conditions like Crohn’s disease, ulcerative colitis, rheumatoid arthritis, etc.

Genetic Factors


The most well known genetic risk factor for AD, in general, is the ApoE gene, specifically with the ε4 allele (ApoE-4). Briefly, alleles are variants of a gene controlling the same trait and occupying the same specific region on a chromosome. We each inherit one allele from each parent, and the combination of those alleles is what creates our unique characteristics.

The most common allele is ε3 (ApoE-3), which is found in more than half of the general population and has a lower risk for AD. This risk goes up if you inherit one copy of ApoE-4 from a parent, and the highest risk for dementia comes from receiving copies of the ε4 allele from both parents, written as ApoE4,4.

Surprisingly, studies indicate that there is a genetic susceptibility to the effects of a head injury. In other words, if you take multiple different people with the same head trauma, some will develop AD while others will not. A major determinant in this process appears to be the ApoE gene once again. Those with at least one copy of the ε4 allele (ApoE4) have been shown to be at increased risk of AD from brain trauma than those who only have the ε2 or ε3 alleles. (8)

Lab Indications


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

Abnormal lab findings in the traumatic subtype of AD can include some or all of the following:

  • Elevated HS CRP or High Sensitivity C-Reactive Protein (>1 mg/L) – marker of both generalized as well as brain-specific inflammation.
  • Markers of increased intestinal permeability (aka leaky gut)
  • Presence of zonulin and/or occludin antibodies
  • Presence of lipopolysaccharide (LPS) antibodies
  • Presence of actomyosin antibodies
  • Antibodies to Foods Cross-Reactive to Amyloid-Beta
    • Egg Yolks
    • Lentil Lectin + Pea Lectin
    • Tuna
    • Hazelnut Vicilin + Cashew Vicilin
    • Scallops + Squid
    • Caseins
    • Alpha-Gliadin + Gliadin Toxic Peptide (gluten-related antibodies)
    • Non-Gluten Wheat Proteins
  • Markers of blood brain barrier permeability (aka leaky brain)
    • Presence of tau protein antibodies
    • Presence of Rabaptin-5 + Presenilin antibodies
    • Presence of Alpha-Synuclein antibodies
    • Blood-Brain Barrier Protein + Claudin-5 antibodies
    • Antibodies to Aquaporins
    • Antibodies to Neurofilament Proteins

MRIs typically will show evidence of trauma in the brain, which include tiny areas of bleeding (called microhemorrhages), diffuse axonal injury, or a softening or loss of brain tissue, called encephalomalacia. The extent of diffuse axonal injury is correlated with the severity of traumatic brain injury depending on location. Stage 1 involves the frontal and temporal lobes, stage 2 extends into the corpus callosum, and stage 3 involves the dorsolateral midbrain and upper pons. (9)

Alzheimer’s Prevention Articles

1.  Morissette, M. P., Prior, H. J., Tate, R. B., Wade, J., & Leiter, J. R. (2020). Associations between concussion and risk of diagnosis of psychological and neurological disorders: a retrospective population-based cohort study. Family medicine and community health, 8(3).
2.  2020 Alzheimer’s Disease Facts and Figures.
3.  Barnes DE, Byers AL, Gardner RC Seal KH, Boscardin WJ, Yaffe K. Association of mild traumatic brain injury with and without loss of consciousness with dementia in U.S. military veterans. JAMA Neurol 2018;75(9):1055-61.
4.  LoBue C, Wadsworth H, Wilmoth K, Clem M, Hart J Jr, Womack KB. Traumatic brain injury history is associated with earlier age of onset of Alzheimer’s disease. Clin Neuropsychol 2017;31(1):85-98.
5.  Fakhran, S., Yaeger, K., & Alhilali, L. (2013). Symptomatic white matter changes in mild traumatic brain injury resemble pathologic features of early Alzheimer dementia. Radiology, 269(1), 249-257.
7.  Katzenberger, R. J., Ganetzky, B., & Wassarman, D. A. (2015). The gut reaction to traumatic brain injury. Fly, 9(2), 68-74.
8.  Nicoll, J. A., Roberts, G. W., & Graham, D. I. (1995). Apolipoprotein E ε4 allele is associated with deposition of amyloid β-protein following head injury. Nature medicine, 1(2), 135-137.
9.  Shetty, T., Raince, A., Manning, E., & Tsiouris, A. J. (2016). Imaging in chronic traumatic encephalopathy and traumatic brain injury. Sports Health, 8(1), 26-36.