The Risk of Alzheimer’s Dementia after COVID-19

This article discusses the alarmingly high possibility of Alzheimer’s disease in certain groups of people after a COVID-19 infection.

Alzheimer’s disease is a brain disease that causes the brain to shrink and brain cells to die eventually. It is the most common cause of dementia, the gradual decline in memory, thinking, behavior, and social skills.

Alzheimer’s disease shortens life. According to a meta-analysis that included 63,125 individuals with dementia, the mean survival time for people with Alzheimer’s disease was 5.8 years.

The featured study that links COVID-19 and Alzheimer’s dementia is from Case Western Reserve University scientists and the National Institute of Health.[1]

The source of their data is the TriNetX Analytics Platform which contains over 95 million patients. It includes inpatient and outpatient visits from 68 healthcare organizations, representing 28% of the US population from 50 states.

At first, they selected subjects that had COVID-19 and with no diagnosis of Alzheimer’s disease in the beginning but were diagnosed with Alzheimer’s within 360 days.

They found 410,478 subjects with COVID-19. The same number of subjects who did not have COVID-19 is the control group. The study period is from February 2, 2020 –May 30, 2021.

The study and control groups were matched using propensity-score matching by

Age
Ethnicity (Hispanic, non-Hispanic)
Race (Asian, Black, White)
Comorbidities (hypertension, overweight, obesity, diabetes, depression, smoking, hearing loss, traumatic brain injury, and alcohol use)
Education
Occupational exposure
The physical, social, and psychosocial environment
Known risk factors for Alzheimer’s disease.

Propensity score matching reduces or eliminates selection bias in studies by balancing the characteristics of participants between treated and control groups. Using it makes it much easier to match participants with multiple traits.

Matching is essential to avoid the effects of certain variables in the result. Matching assures that the increase in Alzheimer’s after COVID-19 is due to COVID-19 only and not to another factor like having diabetes or being obese.

Results

Those who had COVID-19 have an increased risk of a new Alzheimer’s disease diagnosis by 169% compared to those that did not have COVID-19.

After propensity-score matching, the COVID-19 cohort had an increased risk for a new diagnosis of Alzheimer’s disease compared to matched non-COVID-19 cohort (HR: 1.69, 95% CI: 1.53–1.72).

The groups with the highest risk were women (182% risk) and those ≥ 85 years (189% risk).

The increased risk was observed in populations stratified by age groups (65–74, 75–84, ≥85), gender (women, men), and race or ethnicity (Black, White, Hispanic), with the highest risk in people age ≥85 years (HR: 1.89, 95% CI: 1.73–2.07) and in women (HR: 1.82, 95% CI: 1.69–1.97)

The image below shows the increased risk of being diagnosed with Alzheimer’s disease after COVID-19. I marked the two groups (Women and ≥85 years) with the highest risk.

Source: Association of COVID-19 with New-Onset Alzheimer’s Disease. J Alzheimers Dis. 2022;89(2):411-414.

Another study about memory problems after COVID-19 was done in Norway. This time only memory problems were surveyed and not Alzheimer’s disease.[2]

They found that 11% (72 of 651) of those who had COVID-19 had memory problems compared to only 4% (80 of 3,342) who did not have COVID-19 after a follow-up of 257 days.[2]

What is in the SARS-CoV-2 virus that causes COVID-19 that can lead to memory problems and Alzheimer’s?

Causes of Alzheimer’s after COVID-19

Vanderheiden et al. explained that cognitive problems result from blood-brain barrier disruptions and inflammation in the brain in a SARS-CoV-2 infection. [3]

The SARS-CoV-2 Spike proteins can cross the blood-brain barrier and cause brain inflammation.

Another group proposed that hypoxia or lack of oxygen in a severe SARS-CoV-2 can lead to inflammation, decline, and premature aging of the brain cells. [5]

Charnley et al. identified two segments in the SARS-CoV-2 genome, the Open Reading Frames six and ten (ORF6, ORF10), that can strongly produce amyloids.[4] Amyloid proteins are present in the brain of patients with Alzheimer’s disease.

Nyström and Hammarström found seven protein sequences in the SARS-CoV-2 that can form brain and blood vessels amyloids. The amyloids explain the unusually tough and fibrous clots seen in autopsied patients. [6]

I discussed that paper in The SARS-CoV-2 spike protein could form amyloids seen in the lung, blood, and nervous system disorders.

And the autopsy findings at — New and Alarming Autopsy Findings After the COVID Shots

Baazaoui et al. suggest after a review of the literature that COVID-19 leads to the development and acceleration of prions or misfolded proteins commonly found in Alzheimer’s and Parkinson’s. [7]

Based on their research, Nuovo et al. showed that the worsening symptoms of Alzheimer’s disease patients in a SARS-CoV-2 infection are due to microvascular damage superimposed on the plaques and tangles already in the brain.[9]

The inflammation is due to the S1 and S2 subunits of the spike protein of the SARS-CoV-2. Interestingly, these changes are not seen in a SARS infection. [9]

Nuovo et al. added that the effect of the spike protein in the brain is present using a high dose of spike proteins present in an infection but not in a low dose present in the COVID-19 shots. [9]

Effects of lockdowns

Not all can be blamed entirely on the COVID-19 virus. Bakker et al. found that memory clinic patients, specifically those in pre-dementia stages, showed faster memory decline during the COVID-19 lockdown. This provided evidence that lockdown regulations had a deleterious effect on brain health. [8]

They explained that some people may have amyloids and prions in their brains but do not manifest as dementia. That’s because an everyday and structured life enables them to cope with the disease.

However, social changes from lockdowns resulting from a lack of contact with their family and friends, the disruption of routine schedules, and social isolation can act as a “second hit” and bring out or worsen a hidden Alzheimer’s disease. [8]

This observation was also noticed by geriatricians that I know.

What to do?

Consulting with a specialist is of immense help. A geriatrician specializes in the complex care of people with neurodegenerative diseases. They look at the whole picture at home and work with social workers, pharmacists, and psychologists.

Nattokinase is an over-the-counter supplement that can dissolve amyloids and prions. Nattokinase Degrades Amyloids and Prions

I tried it once on someone I know I suspected of slowly developing Parkinson’s disease because of his slow movement, emotionless facial expression, or blunt affect and stiffness. It worked for him, and he is back to his usual self.

I told that story in — Parkinsonism resolved by Nattokinase.

Don’t Get Sick!

Knowledge about Covid-19 is rapidly evolving. Stay current by subscribing. Feel free to share and like.

Follow me on Gettr, Truth Social, Gab, Parler, Twitter, Facebook, Follow, and Telegram.

If you find value in this website, please consider buying a coffee to show your support.

Related:

References:

Wang L, Davis PB, Volkow ND, Berger NA, Kaelber DC, Xu R. Association of COVID-19 with New-Onset Alzheimer’s Disease. J Alzheimers Dis. 2022;89(2):411-414. doi: 10.3233/JAD-220717. PMID: 35912749.
Søraas A et al. (2021) ) Self-reported memory problems eight months after COVID-19 infection. JAMA Netw Open 4: e2118717.
Vanderheiden A, Klein RS. Neuroinflammation and COVID-19. Curr Opin Neurobiol. 2022 Oct;76:102608. doi: 10.1016/j.conb.2022.102608. Epub 2022 Jun 29. PMID: 35863101; PMCID: PMC9239981.
Charnley M, Islam S, Bindra GK, Engwirda J, Ratcliffe J, Zhou J, Mezzenga R, Hulett MD, Han K, Berryman JT, Reynolds NP. Neurotoxic amyloidogenic peptides in the proteome of SARS-COV2: potential implications for neurological symptoms in COVID-19. Nat Commun. 2022 Jun 13;13(1):3387. doi: 10.1038/s41467-022-30932-1. PMID: 35697699; PMCID: PMC9189797.
Sivagurunathan N, Calivarathan L. SARS-CoV-2 Infection to Premature Neuronal Aging and Neurodegenerative Diseases: Is there any Connection with Hypoxia? CNS Neurol Disord Drug Targets. 2023 Apr 18. doi: 10.2174/1871527322666230418114446. Epub ahead of print. PMID: 37073650.
Sofie Nyström and Per Hammarström. Amyloidogenesis of SARS-CoV-2 Spike Protein. Journal of the American Chemical Society 2022 144 (20), 8945-8950
DOI: 10.1021/jacs.2c03925
Baazaoui, Narjes and Iqbal, Khalid. ‘COVID-19 and Neurodegenerative Diseases: Prion-Like Spread and Long-Term Consequences’. 1 Jan. 2022 : 399 – 416.
Bakker ED, van der Pas SL, Zwan MD, Gillissen F, Bouwman FH, Scheltens P, van der Flier WM, van Maurik IS. Steeper memory decline after COVID-19 lockdown measures. Alzheimers Res Ther. 2023 Apr 15;15(1):81. doi: 10.1186/s13195-023-01226-5. PMID: 37061745; PMCID: PMC10104769.
Nuovo GJ, Suster D, Sawant D, Mishra A, Michaille JJ, Tili E. The amplification of CNS damage in Alzheimer’s disease due to SARS-CoV2 infection. Ann Diagn Pathol. 2022 Dec;61:152057. doi: 10.1016/j.anndiagpath.2022.152057. Epub 2022 Oct 28. PMID: 36334414; PMCID: PMC9616485.

As an Amazon Associate, I earn from qualifying purchases.