Does Covid-19 cause memory loss?

Curiosity has striked amongst the scientific research community of the neurological
manifestations from coronavirus, after 22% of COVID-19 recoveries complained of
experiencing memory loss. Although the virus can enter the body via many routes, it can only
bind and infect a host cell with an angiotensin-converting enzyme 2 (ACE-2) receptor molecule
as depicted in Figure 1 (Butowt and von Bartheld, 2022). The lung has high amounts of this
receptor, justifying why the virus primarily causes respiratory symptoms. However, recent
studies observed that the cranial - skull excluding the lower jaw - nerve, nervus terminalis
contains ACE-2 receptors and connects to the hypothalamus of the brain which keeps the
suggestion of covid-19 causing memory loss within the realm of possibilities (Butowt and von
Bartheld, 2022).

Figure 1. ACE-2 acts as a receptor for the coronavirus

(scientifically referred as SARS-CoV-2) and enables it to
infect the host cell (The Conversation, 2020).

ACE-2 has a major contribution to regulating chemicals vital in neurogenesis, cognition and
prevention of neurodegeneration. Coronavirus promotes neurodegeneration by the
neuroinflammation derived from the immune activation in response to its inhibiting effect on
ACE-2 enzymes and the chemicals associated with neuronal growth and survival (Rudnicka-
Drożak et al., 2023). The hippocampus is a segment of the brain that harbours neural stem cells
in adults and plays a crucial role in learning as well as memory (Radhakrishnan and Kandasamy,
2022). Coronavirus can also invade the ACE-2 facilitating hippocampus through the nervus
terminalis and elicit neuronal loss in its regions labeled cornu ammonis 1 and 2 (Klein et al.,
2021). Neurodegeneration suppresses the neural stem cell functional capacity in these
hippocampal areas, compromising the ability to store long-term memories and a sense of spatial
memory. This hippocampal neurodegeneration is amplified when the blood-brain barrier (BBB) -
the brain's protective mechanism against toxins by the tight packing of neuronal cells - is
impaired by the overflow of coronavirus-induced inflammation chemicals (Radhakrishnan and
Kandasamy, 2022).

Shockingly, COVID-19 patients who suffer dementia have a 30% higher mortality rate than
those without, and Alzheimer’s disease (AD) represents 60% of all dementia cases (Chen et al.,
2022). Dementia is a case of irreversible cognitive deterioration associated with memory loss and
these patients are more susceptible to being infected by coronavirus. This stems from the fact
that AD patients have enhanced ACE-2 expressions in the hippocampus which enables a higher
viral entry into the hippocampal cells (Ciaccio et al., 2021). AD derives from a dysfunctional
BBB that prevents glucose from reaching the brain and the clearing away of neurotoxins triggers
immune activation causing uncontrollable neuroinflammation which is characteristic of
neurodegeneration (Kinney et al., 2018). Coronavrius can inhibit the expression of ACE-2,
causing exacerbation of cognitive impairment in AD patients and amplification of the
neurodegenerative process (Villa et al., 2022). Thus, coronavirus is not only more likely to occur
in AD patients, but can also accelerate its neurodegenerative process in the hippocampus, further
augmenting its memory loss implication.

COVID-19 has definitely left a neurological mark regardless of previous neurodegenerative

disease history. The neurodegeneration that coronavirus is proven to instigate in those infected
by the virus causes the lack of ability to recall previous memory and form new long-term
memories. COVID-19 has definitely impaired the memory of its hosts.
Reference list

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