From long COVID to neurodegeneration, 2025, Carpio-Orantes et al

[forestglip]

From long COVID to neurodegeneration

Carpio-Orantes, Luis Del

No abstract. Snippets:

[SARS-CoV-2] has a great predilection for the nervous system, being a neuroinvasive virus that uses various routes such as olfactory pathway, ophthalmic pathway, choroid plexuses, enteric nervous system and the disruption of the blood–brain barrier (BBB); once installed in the nervous system it begins with a great neurotropism that will finally culminate in great neurovirulence, conditioning various pathological conditions.

The main mechanisms of cognitive dysfunction are viral persistence, immunothrombosis, fusion of neurons with glial cells, neuroinflammation, decreased neurogenesis, hypocortisolism due to dysfunction of the hypothalamus–pituitary axis, and vagal dysfunction induced by dysbiosis.[1-3]

Similarly, neuroimaging studies have shown that there is severe diffuse cortical hypometabolism in these patients, and special studies such as PET-PBR28 have revealed neuroinflammation, as well as associated vascular damage.

Currently, research is focusing on neurodegeneration followed by neuroinflammation, which is leading to a higher prevalence of neurodegenerative diseases associated with Long COVID, mainly: Alzheimer’s disease, Parkinson’s disease, dementia, amyotrophic lateral sclerosis, multiple sclerosis and Huntington’s disease. Similarly, cases of neurodegeneration similar to prion diseases and even cases of prion diseases (mainly Creutzfeldt Jakob disease secondary to COVID-19) are beginning to be seen, so the control measures for these chronic and degenerative diseases must be from the acute stages of COVID-19, preventing the inflammation caused by viremia from becoming chronic and affecting the organs, mainly the nervous system, and preventive actions such as vaccination and various anti-inflammatory drugs such as temelimab, baricitinib, as well as antivirals for viral persistence, should also be implemented.[7,8]

Web | DOI | PMC | PDF | Brain Circulation | Commentary | Jan-Mar 2025

 

[forestglip]

Response to the above:

There is currently no evidence that long-COVID-19 leads to neurodegenerative diseases such as SDAT, amyotrophic lateral sclerosis, or Parkinson’s disease

Finsterer, Josef

No abstract, snippets:

First, prolonged COVID-19 is rarely associated with structural or functional abnormalities in the nervous system.[2,3]

Second, SARS-CoV-2 has rarely been detected in the cerebrospinal fluid of patients with cerebral involvement during acute infection. Third, although virus particles were found in all brain regions in COVID-19 patients at autopsy, these regions show little inflammation or virus cytopathology.

Fourth, there are no studies that clearly demonstrate that the prevalence of SDAT, ALS, MS, HD, or PD has actually increased since the end of the pandemic.

Currently, there is not much evidence that long-COVID-19 is due to venous sinus thrombosis (VST), pituitary dysfunction, or vagal dysfunction.

Hypometabolism in certain brain regions (e.g., olfactory bulbs) can hardly explain the general symptoms of long COVID-19 (impaired memory, concentration, cognition, executive functions, fatigue, and exercise intolerance).

There is also little evidence that the skeletal muscles are generally affected in long-COVID-19 and are therefore responsible for fatigue as one of the main symptoms.

To summarize, some of the statements in the index study are speculative and not supported by evidence. There is currently no proven case of a patient with long COVID-19 who has developed SDAT, ALS, or prion disease.

Web | DOI | Brain Circulation | December 2025

 

[Utsikt]

From a few minutes of googling:

https://www.prd-journal.com/article/S1353-8020(23)00156-6/fulltext

After propensity score matching, we found significantly increased odds of new onset Parkinson disease in the COVID-19 cohort at three, six, nine, and twelve months from the index event, with peak odds ratio at six months. After twelve months there is no significant difference between the COVID-19 group and non-COVID-19 group.

Frontiers | Frequency of Neurological Diseases After COVID-19, Influenza A/B and Bacterial Pneumonia

Introduction. COVID-19 might affect the incidence of specific neurological diseases, but it is unknown if this differs from the risk following other infectio...

www.frontiersin.org

In total, 919,731 individuals were tested for COVID-19, of whom 43,375 tested positive (35,362 outpatients, 8,013 inpatients). Compared to COVID-negative outpatients, COVID-19 positive outpatients had an increased RR of Alzheimer's disease (RR = 3.5; 95%CI: 2.2–5.5) and Parkinson's disease (RR = 2.6; 95%CI: 1.7–4.0), ischemic stroke (RR = 2.7; 95%CI: 2.3–3.2) and intracerebral hemorrhage (RR = 4.8; 95%CI: 1.8–12.9).

However, when comparing to other respiratory tract infections, only the RR for ischemic stroke was increased among inpatients with COVID-19 when comparing to inpatients with influenza (RR = 1.7; 95%CI: 1.2–2.4) and only for those >80 years of age when comparing to inpatients with bacterial pneumonia (RR = 2.7; 95%CI: 1.2–6.2).

Frequencies of multiple sclerosis, myasthenia gravis, Guillain-Barré syndrome and narcolepsy did not differ after COVID-19, influenza and bacterial pneumonia.

 

[PageofME]

I have met two seriously incapacitated LC patients – both with fatigue but without PEM – whose symptoms – I thought – could be best explained by a short and hefty brain inflammation. One of them actually half a year later did have a neurologist that confirmed that not only her symptoms but also her brain images strongly hinted at that.

Doctors know for decades that there are many viruses that can provoke a brain inflammation in rare cases even if neurons are not their primary territory. If you have a pandemic you get many cases.

Influenza is the most notorious, I believe. It has been known for decades that it can leave patients severely incapacitated for life sometimes.

This is a rant:

I can't understand how it is possible that researchers are still discussing whether it could be possible at all that there is an LC subgroup that had Covid-19 brain inflammation.

Where should the severe neurological problems and the heavy fatigue come from if not from brain inflammation? I rather think not that we can blame Santa for this.