Can a 19-Year-Old Really Get Alzheimer’s Disease?
I recently read an article in a medical journal reporting that neurologists in China diagnosed in 19-year-old man with probable Alzheimer’s disease in 2023. This man’s memory decline started when he was only 17, and kept progressing. How is this diagnosis even possible? Time for the Medical Detective to get to work.
Establishing an Alzheimer’s Diagnosis
The Chinese neurologists did an F-18 PET (positron emission tomography) scan, which looks at the brain’s metabolic functions. It’s frequently done to try to establish whether there are deposits of amyloid plaques in the brain, one of the hallmark features of Alzheimer’s. This 19-year-old’s scan showed atrophy of the part of the brain responsible for memory (the hippocampus), with low metabolism (hypometabolism) in the bilateral temporal lobes. These are changes that can be seen with Alzheimer’s, but they can also be seen with many other conditions (I’m sure you know where this is going…!) as you will soon see. And after they did a spinal tap to evaluate the fluid surrounding the brain, they found an increased concentration of a common Alzheimer’s marker, called p–tau 181, along with a decreased amyloid-β 42/40 ratio, which is another strong Alzheimer's marker and can be detected early in the disease progression, even before clinical dementia occurs. But here’s the rub. With whole genome sequencing (doing an extensive genetic evaluation), none of the usual gene mutations or Alzheimer’s were identified.
So why did they make this diagnosis they came up with? Without finding potential explanations that can lead to viable treatment, this young man’s life will be destroyed. Let’s examine at some much more plausible hypotheses for the root cause of severe memory loss in a 19-year-old.
Do you suffer from memory loss and concentration problems?
This list gives you the most common variables proven to have been associated with memory loss and Alzheimer’s dementia:
Infections: spirochetes including Lyme disease, Borrelia burgdorferi, Herpes viruses (HSV1, 2, HHV 7, HHV 8), Chlamydia pneumonia, Porphymonas gingivalis, H. Pylori, Bartonella, Propionibacterium, Covid, Candida albicans, Toxoplasma
Environmental toxins (pesticides, heavy metals)
Mitochondrial dysfunction
Microbiome abnormalities
Hormonal deficiencies (sex hormones, thyroid, insulin resistance, hypoglycemia)
Sleep disorders (Delayed Sleep Phase Syndrome, Obstructive Sleep Apnea)
Medication side effects (PPIs, statins, psychiatric meds, anti-cholinergic drugs)
Vitamin deficiencies (B vitamins, Vitamin D)
Genetics
Alcohol disorder
Low or high blood pressure (POTS or hypertension)
Autoimmunity (PANS/PANDAS, Autoimmune encephalopathy)
Now take a look at the 16 points on the MSIDS map that have all been associated with chronic inflammation and memory/concentration problems:
16 Point MSIDS Map: Sources of Inflammation and Downstream Effects Associated with Chronic Cognitive Dysfunction:
Primary Sources
1) Chronic infections
A. bacteria, i.e., spirochetes like Lyme disease, Bartonella spp., porphymonas gingivalis, H. pylori Propionibacterium…
B. viruses, i.e., herpes viruses, COVID
C. parasites, i.e., Babesia, Malaria, Toxoplasma, Echinococcosis (hydatidosis), Schistosomiasis, Paragonimiasis, Toxocariasis, Onchocerciasis
D. fungi, i.e., Aspergillus, Cryptococcus, Candida, Mucorales, dematiaceous molds, and dimorphic endemic fungi
2) G.I.: Dysbiosis of intestinal bacteria
3) G.I.: Leaky gut with food allergies and sensitivities/mast cell activation
4) Sleep disorders: lack of proper sleep (sleep apnea, infections with DSPS, shift worker syndrome, menopause, BPH) can lead to elevated IL-6, an inflammatory cytokine associated with neuroinflammation
5) Environmental toxins (heavy metals, mold, pesticides, VOS’s, etc.)
6) Nutritional deficiencies (zinc, copper, magnesium; vitamin deficiencies, including B1, B6, B12, folate, vitamin D)
7) Nutritional overload (copper, Wilson’s disease; iron, hemochromatosis)
Downstream Effects
8) Endocrine disorders: low testosterone, menopause, low adrenal function, hypothyroidism, low blood glucose
9, 10) Neurological, Psychological dysfunction: strokes, PTSD with trauma, amyloid/tau buildup, tumors
11) POTS/dysautonomia with low blood pressure decreasing cerebral perfusion
12) Mitochondrial Dysfunction: genetic or acquired, affects all organ systems including memory/concentration
13) Pain Syndromes: pain decreases cognitive processing; can affect long-term memory, selective attention, processing speed, and executive functioning
14) Liver Dysfunction: cirrhosis or fatty liver with elevated ammonia, severe hepatitis B or C infection, alcohol abuse, autoimmune hepatitis, bile duct disorders, some medications
15) Autoimmune phenomenon (PANS/PANDAS, AI encephalopathy)
16) Medication side effects: i.e., benzodiazepines, opioids, antipsychotics, anticholinergics, antiepileptics
You will notice that the two lists completely overlap. The majority of the variables found on the 16-point MSIDS map associated with chronic inflammation can cause memory/concentration problems with poor cognition. Although association does not prove causality, there is now accumulating scientific evidence linking Alzheimer’s disease to spirochetal infections like Lyme disease as well as to other infections (such as viruses). One 2022 peer-reviewed article indicated that Borrelia burgdorferi (the bacteria causing Lyme disease) co-localizes with amyloid markers in Alzheimer's disease brain tissues. The Journal of Alzheimer’s Disease had previously shown that Lyme disease is a potential factor causing dementia, and has been shown to be associated with chronic inflammation in the brain that can lead to amyloid production.
Potential Causes of Low Metabolism in the Brain’s Bilateral Temporal Lobes
This was one of the findings that led the neurologists to suspect early Alzheimer’s. Here are other potential causes:
1. Lyme disease: When F-18 PET scans were done by neurologists in 23 Lyme disease patients years ago, the most striking finding was hypometabolism in the temporal lobes in 17/23 (74%) patients. The involvement of the temporal lobes is likely associated with the memory disturbances described in many of these patients. Lyme disease has now affected 14.5% of the world’s population (1/7 people) and is a growing problem in China. I discussed this with scientists from the Chinese government over 10 years ago when I was invited to lecture there, and they told me many patients were presenting with the typical EM (erythema migrans) rashes. Spirochetal infections can cause temporal lobe dysfunction and amyloid production, as you will see in the description below
2. Syphilis: another spirochetal infection
3. Flavivirus infections: these include dengue fever, Zika virus, yellow fever, and Powassan encephalitis (a tick-borne infection)
4. Other viruses: Herpes virus infections and HHV6
5. Fungal infections
6. Seizure disorders: one of the causes of new onset seizures is a Bartonella infection. Of the 20 or so documented Bartonella species, 9 cause neurological diseases. One of the most common symptoms of Bartonella is memory loss
7. Metabolic diseases: a relatively rare genetic disease can cause bilateral temporal lobe dysfunction, due to a pathway in the liver that doesn’t work properly (the ornithine cycle) along with elevated levels of ammonia. This will cause memory problems similar to someone with late-stage cirrhosis of the liver
Potential Causes of Elevated Levels of p–tau 181 and a Decreased Amyloid-β 42/40 Ratio
This was the other finding that led the neurologists to their Alzheimer’s diagnosis. What else causes them?
1. Traumatic Brain Injury (TBI): This can elevate p-tau 181. Many young people have TBI from sports injuries that can lead to neurodegeneration decades later, if severe enough. (Explaining why football and contact sports are re-evaluating how they deal with concussions on and off the field.)
2. Different neurodegenerative diseases: these include frontotemporal dementia with Parkinson’s disease and ALS. Pesticide exposure has now been linked to Parkinson’s disease, and there are ALS patients who have a Lyme-induced ALS presentation that responds to antibiotics and is not related to genetic factors.
3. Patients without amyloid pathology can have a decreased amyloid-β 42/40 ratio: Although elevated levels of p–tau 181 are seen in those with a high amyloid burden (like Alzheimer’s), amyloid usually comes first in the pathological process, with deposits happening over decades before tau proteins occur. The amyloid hypothesis indicates that amyloid-beta clusters appear first and are followed by a surge in abnormal tau once amyloid-beta has accumulated to a certain level—but a 19-year-old normally wouldn’t be old enough for this to happen. Recent research is in fact questioning the amyloid hypothesis altogether, with studies among older adults across the Alzheimer’s pathological spectrum showing that many more individuals show PET scan evidence of amyloid beta pathology in the absence of tau pathology than the converse.
4. Amyloid beta is antimicrobial: many bacteria form amyloid to protect themselves by using it to strengthen their biofilms. Cells can produce amyloid beta as an anti-microbial response to confer increased resistance against both bacteria and viruses. So, a high amyloid burden can be seen in those with chronic infections (like Lyme disease), as mentioned earlier, since amyloid helps control infections!
A Different Marker of p-tau, p-tau231 Is a Better Early Indicator of Alzheimer's Disease
The Chinese neurologists checked for p-tau181, but there is a better marker for early Alzheimer’s. It is called p-tau 231. A recent Lancet article found that “All CSF p-tau biomarkers were accurate predictors of cognitive impairment, but CSF p-tau217 demonstrated the largest fold-changes in AD patients in comparison to non-AD dementias and cognitively unimpaired individuals.”
In other words, we can have p-tau in our spinal fluid when we are cognitively impaired, but head trauma can cause the same elevations. Not all p-tau is due to Alzheimer’s disease. In fact, a growing body of evidence suggests that free radical/oxidative stress is one of the reasons for tauopathies—a high burden of tau in our central nervous system. More research needs to be done on other factors that can cause elevations in p-tau, not just Alzheimer’s. For example, mitochondrial dysfunction and impairment of the energy-producing organelles in our cells can increase p-tau. I see mitochondrial dysfunction in at least one-third of all chronic Lyme patients, and it’s also present in many chronic fatiguing illnesses.
Diagnosis and Initial Testing for Memory/Concentration Problems
To establish the potential causes/testing that should be done in a young person with mild to moderate cognitive impairment, we need to go back to the 16-point MSIDS model. The likelihood of finding a positive test is based on the clinical history and symptoms, travel history, physical examination, and underlying risk factors. An initial laboratory work-up would include getting a CBC (complete blood count), CMP (comprehensive metabolic profile; electrolytes, liver, and kidney function), fasting lipid profile and EKG, sedimentation rate (ESR), syphilis serology (VDRL), Lyme testing (ELISA, C6 ELISA, Immunoblots, IgM/IgG), Bartonella testing (Immunoblots, FISH/RNA test) as well as basic hormones (thyroid), vitamin levels (B12, MMA), and heavy metals in the blood (Hg, Pb, AL, As, Cd). I would also do sitting and standing blood pressure and pulse rates (to rule out POTS/dysautonomia) and review of medications that can adversely affect cognition. The American Academy of Neurology also recommends checking drug levels, HIV testing, and a 24-hour urine testing for heavy metals apart from considering a chest X-Ray, CT/MRI of the head, EEG (electroencephalogram), PET scan, and if indicated, spinal tap to check the cerebrospinal fluid.
Final Thoughts
The Medical Detective would never accept the diagnosis of early Alzheimer’s in a 19-year-old patient without ruling out most of the above medical problems. Lyme, Bartonella, mold, and massive loads of environmental toxins are getting into our bodies every day—all of which can cause cognitive problems. And/or did this patient have a traumatic brain injury from sports?
There is an old saying in medicine. If you hear hoofbeats outside the window, think of horses before zebras. An Alzheimer’s diagnosis in a 19-year-old male is a zebra. Don’t let lab and radiological testing drive a diagnosis when the burden of proof is likely to be found in much more common reasons for cognitive issues.
References:
1. Jia J, Zhang Y, Shi Y, et al. A 19-Year-Old Adolescent with Probable Alzheimer’s Disease. Journal of Alzheimer’s Disease. 2023;91(3):1–8.