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Conversations with Julián Benito León and Souvik Dubey: How Covid-19 accelerates cognitive decline in dementia patients.

A recent study published in the Journal of Alzheimer’s Disease Reports revealed that SARS-CoV-2 infection significantly accelerates cognitive decline in dementia patients. The researchers found that after COVID-19 infection, all forms of dementia progressed rapidly, and differences between subtypes became less clear.

In addition, the nature of each dementia type changed, with both degenerative and vascular dementias displaying mixed dementia characteristics. The study, which suggests that dementia-compromised brains have little resilience against further damage, led the team to propose ‘FADE-IN MEMORY’ as a new term for describing the range of cognitive impairments post-COVID-19.

Julián Benito León and Souvik Dubey, two of the researchers involved in the study, discussed their findings with SCINQ.

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What inspired you to study the impact of SARS-CoV-2 on cognitive functioning in patients with pre-existing dementia?

Recent studies have already shown the deleterious impact of COVID-19 on cognition in previously normal individuals without dementia. We hypothesized that COVID-19 must have some definitive impact on the already compromised brain in patients with pre-existing dementia. The multifactorial association has already been proposed and proved. 

How were the patients selected for this study and why did you choose to focus on these particular subtypes of dementia?

We have been working on patients with dementia with diverse etiologies. To make the patients’ group homogeneous, we only took those patients already suffering from degenerative dementia like Alzheimer’s dementia, frontotemporal dementia, and vascular dementia. Many had COVID-19 and complained of further deterioration of their cognitive abilities. 

Could you elaborate on the observed changes in white matter hyperintensities in patients post-COVID-19 and their significance?

White matter intensity changes have been observed in most patients, which may have an underlying diverse pathophysiological basis, among which microvascular ischemia and inflammation are the two most important considerations hypothesized. White matter involvement might be responsible for decreased attention, mood changes (depression), executive function impairment, poor information processing speed, and subcortical-type memory impairment. 

What connection did you find between COVID-19 and the increase in fatigue and depression scores in these patients?

The presence of fatigue and depression is quite characteristic in patients with pre-existing dementia with COVID-19. However, it still requires large studies to conclude as fatigue and depression are also seen in a large number of patients following COVID-19 without dementia. Multifactorial causation might be one explanation. We hypothesized similarities between the multiple sclerosis brain with white matter intensity changes, cognitive impairments, and presence of depression and fatigue and post COVID-19 brain with white matter intensity changes, cognitive impairments, and presence of fatigue and depression, which might be indicative of shared pathophysiological basis of inflammation underneath. 

Can you discuss how COVID-19 affected the Frontal Assessment Battery and Addenbrooke’s Cognitive Examination scores in these patients?

We observed objective attention/concentration difficulties, executive dysfunctions, slowed information processing speed, and sub-cortical type memory impairments in all patients one year after SARS-CoV-2 infection. The mean Frontal Assessment Battery and Addenbrooke’s Cognitive Examination scores significantly worsened following COVID-19 infection in patients with pre-existing dementia. However, more research is needed to understand the impact of COVID-19 on cognitive functioning in patients with pre-existing dementia.

How does the term “FADE-IN MEMORY” better reflect the cognitive sequelae observed in patients with pre-existing dementia post-COVID-19?

The term “FADE-IN MEMORY” is proposed to reflect better the cognitive sequelae observed in patients with pre-existing dementia post-COVID-19. The term stands for fatigue, decreased Fluency, Attention deficit, Depression, Executive dysfunction, slowed Information processing speed, and subcortical Memory impairment. The term is just a codename for easier understanding of the pattern of multidomain cognitive impairments. However, it does not mean that post-COVID-19 cognitive impairments in patients with pre-existing dementia spare other domains. It can involve other domain/s as well, but most commonly involves the domains clubbed together in the codename. 

What do you predict the implications of your findings will be for future dementia research and treatment, especially in the context of COVID-19?

We think that larger studies are needed in this sense. Important limitations of our study are that the number of patients studied is small, and secondly, the pathobiological basis was hypothesized only. Due to overlapping patterns and characteristics of cognitive impairments in various degenerative dementias and post-COVID-19 cognitive impairments, it will be very difficult to subtype dementia clinically in patients with cognitive impairments with a history of COVID-19. 

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