“I want to ask about your view and experience with cognition post COVID shots,” a woman asked me recently. “My husband’s issue started shortly after that. We have also recently learned that he is still producing crazy high antibodies to the SARS COVID spike protein, up to 1700. To our knowledge he has never had COVID and he has tested high antibodies multiple times in the last year.”
She provided additional details, and I asked if I could share because this is part of the chronic immune activation story I’ve been writing about lately. As a reminder, chronic immune activation means the immune system stays switched on — actively signaling and producing inflammation — long after the trigger that provoked it should have been resolved. In my experience with Alzheimer’s prevention and improving cognitive decline, it's almost always more than one trigger keeping it that way.
Two things are tangled together in her description. One is a timing observation: his cognitive symptoms started not long after his vaccine. The other is a lab result that didn’t make sense to her: how can his antibody levels stay this high, tested repeatedly over a year, if he’s never had COVID? That second question is the key to the first.
There isn’t just one kind of COVID antibody test. He’s had spike antibody tests twice, in 2025 and again in 2026, both markedly elevated. Spike antibody tests measure your response to the spike protein, and both infection and vaccination cause that response — a high result doesn’t tell you which one caused it.
When I asked which test he had, it turned out he had both of the tests I asked about. The spike antibody test result was high twice. And he also had a nucleocapsid antibody test, ordered by accident, which turned out to be the additional test needed to provide the clarity she wanted.
This one only comes back positive with actual infection, since vaccines don’t trigger a response to that part of the virus. His came back negative. So there’s no evidence he was ever infected — his high antibody levels are coming from the vaccine, and his immune system hasn’t fully stood down in close to two years.
She also shared that he carries two copies of the APOE4 gene, the strongest known genetic risk factor for Alzheimer’s, and that he’s had elevated TGF-beta1 since 2024, even after mycotoxin-related treatment. She wondered whether his immune system had “gone overboard” on the vaccine because of his genetics.
That’s a smart question.
Why the APOE4 question matters
APOE4 isn’t just about how the body clears cholesterol and amyloid. It also shapes how the immune system responds to a threat in the first place. Some research suggests APOE4 carriers mount stronger, more prolonged inflammatory responses than people without the gene. If true for him, his immune system isn’t malfunctioning — it may be doing what an APOE4/4 immune system is more prone to do.
Ongoing immune activation produces inflammatory signals that circulate through the blood. The brain normally shields itself with the blood-brain barrier, but sustained signals can wear that barrier down, letting inflammation reach the brain's immune cells and keep them on alert.
His high and not declining antibodies suggest the immune system may still be responding to residual spike protein — in his case, from the vaccine, since there's no evidence of infection. That alone doesn't mean it's affecting his cognition. It just means his immune system is still responding to the spike protein, which isn't necessarily abnormal in immunology — though the data on long-term risk from persistent spike protein specifically isn't available yet.
What could still be provoking the immune response? A few possibilities:
Persistent spike protein or vaccine-derived material in his body hasn’t fully cleared
Bystander activation from an unrelated, ongoing immune stressor keeping his whole system alert
Simple individual variation in how long antibody titers stay elevated after any exposure
There’s likely more than one thing going on.
The more things an immune system is activated against at once, the more likely that signaling reaches and affects the brain. A single elevated antibody by itself is one thing. Multiple simultaneous sources of activation are a different situation.
He’s had mold exposure, with remediation for his home in 2023, along with antifungal treatment for the internal mycotoxin burden. Continued elevated TGF-beta1 after treatment could mean re-exposure happened, or that treatment addressed the fungal component without addressing his actual mycotoxin body burden, which is a separate thing to measure.
If his immune system has also been under sustained pressure from mold this whole time, that’s a system already working overtime on a separate front for the same span his spike protein antibody levels have stayed elevated.
It would be interesting to see whether his spike antibody starts declining once his TGF-beta1 normalizes — if both move together, that could fit the bystander activation pattern listed above. If TGF-beta1 normalizes and the spike antibody doesn’t budge, that suggests they’re more independent than connected.
She’s right to keep tabs on this. Sustained high levels of spike protein antibodies are worth taking seriously, and she and her husband have already done a lot of work trying to improve his cognition —
mold remediation, pursuing fungal treatment for the mold, working with their doctor on his testing over time. It also happened to work out well that the test that finally clarified his antibodies was ordered by accident, and turned out to be the most revealing one they could have gotten relative to whether he had COVID or not.
Here’s their good news. He’s improved. The cognitive issues he was having previously, like trouble following TV shows and getting lost driving to familiar places, have gotten better. His current main difficulty is word-finding. He’s also physically active, which is one of the best things you can be for your cognition.
His spike protein antibody level, meanwhile, hasn’t moved across nearly two years of testing. The cognitive improvement appears to line up with the mold treatment, not with any change in his vaccine-related antibody.
Right now, for his cognition specifically, the mold-related piece looks like the active problem, and addressing it is what moved the needle.
The more things a chronically activated immune system is dealing with at once — mold, a latent virus, a vaccine response that hasn’t settled, a leaky gut, a genetic tendency to hold onto all of it — the harder it is for that system to stand down. Each contributor adds to the total load, and the total load determines whether the immune system can quiet itself.
Once you start correctly identifying and addressing what’s actually contributing, even one piece at a time, as this couple as done, things can genuinely get better. His case is proof of that.
What the research actually shows
Researchers reviewed medical records for over six million adults 65 and older and compared new Alzheimer’s diagnoses in the year after COVID-19 infection versus no infection. The numbers were small either way — 0.68% of the COVID group versus 0.35% of the non-COVID group — but that’s roughly double, even after adjusting for age and other risk factors. This doesn’t prove COVID causes Alzheimer’s, and it can’t tell you whether COVID was acting alone or lighting a fire under something already there. But it’s important information at a scale worth taking seriously.
Why persistent activation happens
COVID-19 and the vaccine both provoke a strong immune response that resolves in most people. In a meaningful subset, it doesn’t. Some people continue producing spike protein long after infection clears.
Researchers studying vaccinated people with unresolved symptoms describe a similar pattern of persistent spike protein and ongoing immune dysregulation, with no infection involved at all.
None of this research has isolated the vaccine or the virus as a sufficient cause on its own — none of it looked for other contributing factors. That’s typical: researchers usually look for a single variable, when in something as complex as Alzheimer’s, it’s usually a combination.
In my experience, chronic immune activation is not from one thing. Common overlapping contributors I see:
Mold toxins, sometimes alongside a reactivated latent Lyme infection
A leaky gut, which carries its own ongoing immune response until healed
Elevated antibodies to other viruses, like EBV or HHV6, even without full reactivation
It’s not uncommon for all of those to be in play at the same time.
A chronically activated immune system produces a steady stream of inflammatory cytokines that circulate well beyond the original problem. As mentioned earlier, in the brain, they prime microglia into a persistent defensive state and can break down the blood-brain barrier — the structure meant to keep inflammation out of brain tissue.
Once that barrier is compromised, amyloid production increases, neurons come under sustained stress, and the slow damage that eventually shows up as cognitive decline begins to build.
The specific trigger matters far less than whether the immune system stays switched on long enough for this process to take hold.
It should be reversible if addressed properly, early enough.
If you’re recognizing pieces of your own experience, or your spouse’s, or someone else you love — the next questions I’m exploring in the rest of this post are how you’d actually find out what’s driving it, and what to do about it.