Temporal Association between COVID-19 Infection and Subsequent New-Onset Dementia in Older Adults: A Systematic Review and Meta-Analysis, 2024, Shan+

Temporal Association between COVID-19 Infection and Subsequent New-Onset Dementia in Older Adults: A Systematic Review and Meta-Analysis

Abstract
Background: The relationship between COVID-19 infection and the increased likelihood of older adults developing new-onset dementia (NOD) remains elusive. This review primarily aimed to investigate the potential role of COVID-19 in leading to NOD among older adults aged 60 years and older over various time intervals.

Methods: A thorough search was performed across several databases including MEDLINE/PubMed, PsycINFO, Scopus, medRxiv, and PQDT Global for studies published in English from January 2020 to December 2023. We assessed the risk of developing NOD, using Risk Ratio (RR) for measurement. The control groups were categorized as: (i) a non-COVID cohort with other respiratory infections [control group (C1)]; and (ii) a non-COVID cohort with otherwise unspecified health statuses [control group (C2)]. Follow-up periods were divided into intervals of 3, 6, 12, and 24 months post-COVID. The study protocol was registered with PROSPERO (CRD42023491714).

Results: Our review incorporated 11 studies, encompassing 939,824 post-COVID-19 cases and 6,765,117 controls. The overall pooled analysis revealed a significant link between COVID-19 infection and an increased risk of NOD (RR = 1.58, 95% CI 1.21–2.08). In subgroup analyses, NOD risk was significantly higher in the COVID-19 group compared to C2 at 12 months post-COVID (RR = 1.84, 95% CI 1.41–2.38), but not at 3 (RR = 0.87, 95% CI 0.46–1.65) or 6 months (RR = 1.73, 95% CI 0.72–4.14). Compared to C1, the risk increase was not significantly remarkable at 3 (RR = 0.94, 95% CI 0.35–2.57), 6 (RR = 1.13, 95% CI 1.07–1.20), and 12 months (RR = 1.12, 95% CI 0.91–1.38), and overall (RR = 1.13, 95% CI 0.92–1.38). Female had a significantly higher risk of developing NOD in the COVID-positive group (RR = 1.65, 95% CI 1.53–1.78) and C2 group (RR = 1.33, 95% CI 1.22–1.44). Patients with severe COVID-19, as classified by the American Thoracic Society guidelines, were significantly much more prone to developing NOD than those with non-severe infections (RR = 17.58, 95% CI 10.48–29.49). Cognitive impairment was nearly twice as likely in COVID-19 survivors compared to those uninfected (RR = 1.93, 95% CI 1.52–2.43).

Discussion: COVID-19 infection may be linked to a higher risk of NOD in recovered old adults at the subacute and chronic stages following COVID-19 diagnosis. This risk appears to be on par with that associated with other respiratory infections.

https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4716751

 

How do we know the control groups have never had COVID ?

Post 2021 that's a tall order .
Asymptomatic transmission is common. A year and a half ago my in laws only knew they caught it because someone in their social circle tested themselves, they didn't feel unwell , other than one felt as if a cold was coming on, but didn't develop into anything. Now of course anything is something other than COVID..
This is also an age group who socialise a lot .

Number of infections and new onset dementia would be a good metric ... if we still regularly tested folks, but given society is in total denial that's not a thing.

 

We don't and we can't. Virtually everybody has had Covid, this research will never be causal and at best it will detect some correlations that might not be noise. That'll only change if dementia research can ever unlock some more useful markers.

So if the findings hold water you will see a global increase in diagnoses in the long-run. It will be hard to draw any conclusions from that data though since you'll just be seeing some correlations rather than causations. My guess is in 20 years one will just say that certain pandemics generally cause a certain increase or speed up the development of certain neurodenegerative conditions at a population level (which is similar to what they say about the spanish flu and Parkinsons), some of these effects will be unspecific and apply to all viruses and some viruses will have specific certain effects, which are the ones one should aim to untangle. This is similar to what the authors say "We assume that non-COVID-infected status may act as a protective factor against the development of dementia over time.".

This paper does state quite clearly that "This risk appears to be on par with that associated with other respiratory infections.", which makes it harder to untangle anything. It should be noted they are refering to hospitalised respiratory infections here, whilst the Covid-19 data appears to be all sorts of data. Ideally you'd have hospitalised respiratory infections (+if they had something like the yearly flu vaccine) vs. non-hospitalised respiratory infections (+if they had if they had something like the yearly flu vaccine) vs hospitalised Covid infections for certain variants +no. of vaccines vs non-hospitalised Covid infections for certain variants +no. of vaccines and even then you still have to control for all sorts of other things...

Here they are also only looking at data for people that are of the age 60+, whilst the data for younger age groups might in fact be more interesting, debilitating and revealing and might be where differences lie (Covid-19 long-lasting "brain fog" seems to be reported in particular amongst younger populations when compared to other infections).