Covid-19 primarily impacts older individuals and those with underlying medical conditions such as diabetes, obesity, cardiovascular (heart) disease and hypertension (high blood pressure).
These conditions can compromise the immune system, making these individuals more susceptible to severe infections and complications from the infection. Additionally, previous studies have highlighted that pre-existing dementia is a significant risk factor for increased severity and higher mortality (death) rates in Covid-19 patients.
This is likely due to the fact that individuals with dementia often have other underlying health issues and may struggle to comply with infection prevention measures.
Furthermore, the presence of the apolipoprotein E4 (ApoE4) allele, which is the strongest genetic risk factor for Alzheimer’s disease, has been found to also enhance the risk of severe Covid-19 as it can facilitate the entry of the SARS-CoV-2 virus into cells.
ApoE4 is involved in lipid (fat) metabolism and neuronal (nerve cell) repair, but its presence may exacerbate inflammatory responses and impair immune function, thereby increasing vulnerability to both Alzheimer’s disease and Covid-19.
This genetic link underscores the complex interplay between neurodegenerative diseases and infectious diseases, highlighting the need for tailored healthcare strategies for populations at risk. The presence of the ApoE4 allele gene is also known for elevating the risk of Alzheimer’s disease.
Affecting the brain
The diverse neurological symptoms associated with severe Covid-19 suggest that the SARS-CoV-2 virus can affect the brain through multiple mechanisms. Although Covid-19 affects the respiratory system, many studies have shown that it can indirectly impact the brain by causing hypoxic changes.
Hypoxia – a condition where tissues are deprived of adequate oxygen – is associated with dementia and neuropathological changes, and has been linked to increased amyloid-beta generation. Amyloid-beta proteins are the main component of the characteristic plaques that are found in the brains of Alzheimer’s patients.
As SARS-CoV-2 infection is also associated with hypoxia, the resultant dementia may arise from these indirect effects, rather than from the virus directly affecting the brain. The SARS-CoV-2 virus gains entry into host cells by binding to the angiotensin-converting enzyme 2 (ACE2) receptor on the cell wall.
In individuals with Alzheimer’s disease, ACE2 is overexpressed in the brain, which may facilitate increased viral invasion and exacerbate neurological damage. Moreover, when the SARS-CoV-2 virus binds to and inhibits the ACE2 receptor, it can lead to a reduction in brain-derived neurotrophic factor (BDNF) levels.
BDNF is crucial for the survival, development and function of neurons (nerve cells). Reduced BDNF levels can contribute to neurodegeneration, thereby accelerating the progression of Alzheimer’s disease and other forms of cognitive decline.
This dual impact of increased viral entry and decreased neurotrophic support underscores the potential for more severe neurological consequences in Alzheimer’s patients infected with the SARS-CoV-2 virus.
The virus may also increase the toxicity of amyloid-beta proteins, and its spike protein could promote aggregation by binding to amyloid-beta and other amyloid proteins, potentially exacerbating their toxicity.
This mechanism could explain the accelerated progression of dementia observed in Alzheimer’s patients with Covid-19.
Understanding the link
Dementia encompasses various forms, and some types are known to be associated with infections. Given that Covid-19 and Alzheimer’s disease share common risk factors and pathological features, there are significant public health concerns about the neurological effects of SARS-CoV-2 infection.
Understanding the relationship between these two conditions is crucial for developing effective treatments and preventive strategies.
Research has shown a significant link between Covid-19 and Alzheimer’s disease, with SARS-CoV-2 infections being associated with neuroinflammation, neurodegeneration and long-term cognitive impairment.
Covid-19 has been shown to trigger neuroinflammation – a response characterised by activation of the brain’s immune cells that leads to the release of inflammatory cytokines and other mediators. This inflammatory response can damage neuronal cells and disrupt neural networks, contributing to neurodegeneration.
In the context of Alzheimer’s disease, which is already marked by progressive neurodegeneration and the accumulation of pathological proteins such as amyloid-beta and tau, the added neuroinflammation from a SARS-CoV-2 infection could accelerate these processes, worsening the patient’s cognitive decline.
Indeed, brain scans conducted before and after Covid-19 suggest that the SARS-CoV-2 virus triggers structural changes. These findings suggest that Covid-19 and Alzheimer’s disease may have synergistic effects, where the presence of one condition could potentially exacerbate the severity and progression of the other.
Long Covid is increasingly recognised, particularly among the elderly, and may be associated with amyloids formed by the SARS-CoV-2 virus. The persistence of symptoms beyond the initial infection is still under investigation, and any post-pandemic rise in dementia rates will take time to manifest.
The long-term cognitive impairment observed in Covid-19 patients, often referred to as “brain fog”, includes symptoms such as memory loss, difficulty concentrating and reduced executive function. These symptoms overlap significantly with those seen in Alzheimer’s disease, suggesting a possible overlap in the mechanisms through which Covid-19 impacts brain health.
If Covid-19 follows the patterns seen in other viral-induced dementias and exacerbates Alzheimer’s disease, an increase in the latter’s rates might emerge over time. The effectiveness of Covid-19 vaccination strategies in protecting against dementia remains uncertain.
Preventive strategies
The interaction between Covid-19 and Alzheimer’s disease highlights the importance of further research to elucidate their long-term implications. A particularly critical question is whether the SARS-CoV-2 virus itself causes dementia or if it exacerbates pre-existing dementia.
Future research should focus on understanding the molecular and cellular pathways involved, the potential for shared therapeutic targets, and strategies for early intervention to mitigate the compounded effects of both diseases.
By deepening our understanding of the link between these two conditions, we can better prepare for and manage the potential surge in neurodegenerative conditions following the Covid-19 pandemic.
Although there is no surefire way to prevent Alzheimer’s disease, adopting healthy lifestyle habits can significantly improve the immune system and support brain health, as well as reduce the risk of cognitive decline and potentially lower your risk of this condition.
It’s never too early nor too late to start making positive changes and maintaining a healthy lifestyle. This includes eating a balanced diet rich in fruits, vegetables, whole grains, lean proteins and healthy fats.
In fact, diets like the Mediterranean and DASH diets have been linked to a lower risk of developing dementia. Regular physical activity – aiming for at least 150 minutes of moderate-intensity exercise weekly – improves blood flow to the brain and promotes neuron growth.
Mental stimulation through reading, doing puzzles, learning new skills or playing musical instruments helps maintain cognitive function. Ensuring that you get adequate and restful sleep is crucial, as poor sleep can increase the risk of Alzheimer’s disease.
Staying socially active and managing chronic conditions such as diabetes, hypertension and obesity through lifestyle changes can also reduce dementia risk. Additionally, avoiding smoking and excessive alcohol consumption benefits overall brain health.
By Datuk Dr Nor Ashikin Mokhtar
Published in Star Newspaper, 29 Jul 2024
