HomeENGLISH MAGAZINEIs COVID sharing Alzheimer's threads? The preliminary find-outs

Is COVID sharing Alzheimer’s threads? The preliminary find-outs

In addition to respiratory manifestations, the coronavirus also causes neurological abnormalities with an occurrence rate of 85% in those with Alzheimer’s. Most COVID-19 patients experience neurological symptoms such as headache, anosmia, and hypogeusia before the onset of respiratory symptoms. Additionally, the long-term sequelae of COVID-19 could range from mild cognitive impairment to dementia. Last night a famous television program was broadcast which spoke of “two years of COVID”. The last section of the program was dedicated to the context of senile dementia and the difficulties that the pandemic has imposed on this category of patients. A recent study demonstrated the presence of SARS-CoV2 in the olfactory mucosa and its neuronal projections of coronavirus infected patients. Furthermore, additional routes of entry for the virus have been proposed, such as through the blood brain barrier (BBB) ​​in conditions such as autism and Alzheimer’s disease, but without sufficient evidence of infected immune cells.

But that’s not all: a study published a couple of weeks ago, investigated the potential neurotropic characteristics of the coronavirus in COVID-19 patients with Alzheimer’s, autism, dementia, and those without comorbid conditions. The control group for the study consisted of non-COVID patients with the aforementioned comorbidities. The results indicated that SARS-CoV-2 invaded the lower frontal cortices of five COVID-19 patients: one subject with frontotemporal dementia (FTD), one with Alzheimer’s, two with autism, and one healthy subject without comorbid conditions by infecting neurons and many other cells in the cerebral cortex. The cortices of the two young COVID-19 patients with autism showed the presence of tangles of p-Tau protein. Manifestations such as cellular Aβ (amyloid) accumulation and plaque formation, neuro-inflammation and other cellular phenomena such as tauopathy, senescence, ferroptosis, necroptosis, and apoptosis in COVID-19 patients indicated that the virus improves or induces neuropathology similar to Alzheimer’s disease.

The mature neurons infected with the coronavirus were derived from stem cells of age-matched healthy patients with COVID-19 and those with Alzheimer’s through the ACE2 receptor and a facilitator called neuropilin-1 (NRP1), but the coronavirus did not infected immature neurons. Furthermore, the virus activated an Alzheimer’s-like cellular program in stem cell-derived neurons of healthy COVID-19 patients and enhanced Alzheimer’s phenotypes in Alzheimer’s patients’ neurons. In neurons of COVID-19 infected Alzheimer’s patients, the virus improved and reduced the expression of 25 upregulated and 34 downregulated genes, respectively, by many times. Thus, SARS-CoV2 intensifies Alzheimer’s conditions through altered gene expression, elevated neuroinflammation, and other neurological processes in the neurons of Alzheimer’s patients. Furthermore, the silencing of the first three downregulated genes in human primary neurons, named CryAA2, PSG6, and GJA8, by the coronavirus led to the conversion of healthy human neurons into Alzheimer’s-like neurons during COVID-19.

Permeability of the blood-brain barrier (BBB) is believed to be the primary central nervous system entry route for SARS-CoV2 in patients with autism, as no signs of infiltration of SARS-CoV2 infected immune cells were observed in the current study in the autistic brain. The results of the study were in line with those of previous studies suggesting the manifestations of neurodegenerative features in the brains of COVID-19 patients. Further investigation is needed to illustrate the mechanism by which SARS-CoV-2 elicited Alzheimer’s-like phenotypes. It is safe, however, that the virus-induced neuroinflammation process is a central contributing factor. This is not to say that everyone who has caught COVID will develop senile dementia. However, the infection simulates a degenerative process similar to that induced by beta-amyloid and the fact that the “neuro-COVID” includes symptoms such as confusion, difficulty concentrating and memory problems that precede senile dementia, researchers cannot fail to be concerned about possible future repercussions on public health and health.

  • Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Adviced in this website (in italian)

Il neuro-COVID: come avviene, come si manifesta, si può combattere? (12/01/2022)

Le facce della neuro-infiammazione: dai traumi fino alle reazioni al vaccino anti-COVID (05/01/2022)

Demenza senile: i markers classici sono aspecifici, quelli metabolici forse meglio (14/09/2021)

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Dott. Gianfrancesco Cormaci

Medico Chirurgo, Specialista; PhD. a CoFood s.r.l.
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry residency in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Guardia medica presso strutture private dal 2010 - Detentore di due brevetti sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento enzimaticamente neutralizzata (owner of patents concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (Leader of the R&D for the partnership CoFood s.r.l.) - Autore di articoli su informazione medica e salute sul sito www.medicomunicare.it (Medical/health information on website) - Autore di corsi ECM FAD pubblicizzati sul sito www.salutesicilia.it
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