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COVID-19, the Brain, and Mental Health: Weighing the Direct and Indirect Effects


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Andrew Chen

Register for this webinar! 

July 29, 2020

11:00 AM - 12:00 PM EDT

While COVID-19 is often thought of as primarily a respiratory disease, many neurological symptoms are present in those affected. Societal changes in response to the pandemic, such as social isolation and economic disruption, influence mental health. In this webinar, Alycia Mosley Austin, PhD will discuss recent findings on the direct and indirect implications of COVID-19 on the health and function of the nervous system with David Porteous, PhD and Sandeep Robert Datta, MD PhD

After this webinar, participants will be able to:

  • Describe the effects of the COVID-19 virus on these sense of smell.
  • Identify other possible direct effects of the COVID-19 virus on brain function.
  • Discuss how the social and economic impacts of the COVID-19 pandemic can affect mental health and well-being.
  • Explain why the indirect impacts of COVID-19 on mental health and well-being are not felt equally across groups.
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Andrew Chen

Dr. Datta and Dr. Porteous enjoyed seeing all the questions come in during the webinar, and even though they couldn't answer all of them on air, have written out responses to more of them below.

Dr. Datta's responses:

1.       Do you see independent effects on the other chemical senses?

Some patients have reported disruptions to taste and chemesthesis in addition to changes in their sense of smell. However, it remains difficult to evaluate how independent these effects are. In many cases alterations in the taste of foods can indeed be attributed to changes in olfaction. In other cases, the loss and recovery from these changes in chemosensation may indeed be more independent. Further research is required to understand to what extent the SARS-CoV-2 virus can infect and target all chemosensory systems.

2.       Nice presentations.  For all Panelist, II would like to have thoughts on potential covid-19 triggered endemic of Neuropsychiatric disorders, akin to what happened post Spanish flu (encephalitis lethargica)?

Interesting question. Currently, there is still little evidence that SARS-CoV-2 is can directly infect neurons. There have also been relatively few reports of encephalitis, which occurs more frequently in infection from other viruses (like the H1N1 virus that caused the 1918 pandemic). However, it remains to be seen whether there will be any long-term direct and indirect neurological and neuropsychiatric consequences of COVID-19.

3.       How specific is CK18 for Sars Cov 2 detection in tissue? what is the portion of the coronavirus the marker interacts?

Sorry for not explaining that slide as well as I could have. CK18 is a marker for the supportive sustentacular cells that the SARS-CoV-2 infects in the olfactory epithelium. The antibody detecting SARS-CoV-2 detects the nucleocapsid protein of the virus.

4.       Do we have any animal models developed to study this virus?

Yes, there are a number of non-mouse model organisms, including hamsters, ferrets, cats, and non human primates, that have been used to study SARS-CoV-2. These animals are all susceptible to SARS-CoV-2 infection due to the nature of their ACE2 proteins. In contrast, SARS-CoV-2 is unable to use mouse ACE2 to enter cells. Therefore, researchers already have and are continuing to develop mouse models that express human ACE2. In some cases, these mouse models accurately recapitulate the native expression patterns for ACE2 and will likely be quite useful in our understanding of COVID-19. In contrast, a variety of transgenic mouse models express ACE2 in cells that normally do not, making interpretations of studies that use these models more difficult.

5.       What percentage of COVID infections have anosmia and how early in the infection does it occur?

Literature reports suggest that as many as 50-90% of COVID-19 patients may have some degree of smell loss. Smell loss can be the first symptom to appear, and the median time to symptom onset after SARS-CoV-2 infection is around 5 days.

6.       I had a colleague who reported his anosmia with COVID as so severe that he tested it and could not even smell bleach- has the degree of severity of the anosmia been examined?  This suggests that it might even impact the pain sensation in the trigeminal nerve.

Good point. Indeed, patients have had different degrees of smell loss, as measured both from patient reports and from more objective measures of olfactory testing. Additionally, anosmia has also been shown to sometimes occur with ageusia, as well as with chemesthethetic changes. The trigeminal neurons do not appear to express ACE2 but clinical reports like the one you mentioned do indeed suggest that other chemosensory systems besides the olfactory system might be affected in COVID-19.

7.       Does coronavirus disproportionately affect olfactory sensory of different age groups?  Are patients of greater age more susceptible?

Although the risk for severe illness with COVID-19 increases with age, I am not aware of any studies suggesting that anosmia is worse depending on age. If anything, the median age of COVID-19 patients with smell loss is lower than that of patients with more severe symptoms. Further research is definitely needed to see which symptoms are age-dependent, and why.

8.       Meinhardt, et al, BioRxiv preprint suggests that SARS-CoV-2 is infecting the medulla oblongata via the olfactory infection.  Does Dr. Brann think this is likely, given that he points to the supportive cell infection and not the neuronal cells?

We think it is unlikely, given the current evidence, that neurons and nerves are being directly infected. One possible explanation for positive detection of the virus via RT-PCR in the Meinhardt manuscript is from the infection of vascular supportive cells within the brain regions they sampled. There is no direct data in that paper demonstrating trans-olfactory transfer of virus into the brain.

9.       Is there an opportunity to study Neurogenesis in the Olfactory system in humans post COVID-19 infection?

Neurogenesis has been difficult to study in humans, and there is relatively little work with human nasal biopsy samples, and even less with the human olfactory bulb. There could be opportunities to evaluate markers for neurogenesis in the olfactory systems of post-mortem samples.

10.   Is there any evidence for expression of ACE2 in the subventricular zone?

Not that I am aware of. However, although there are now a number of high-quality datasets from the mouse (and our analyses of the mouse olfactory epithelium yielded similar conclusions our analyses of the human olfactory epithelium), there is still relatively little expression data from most regions in the human brain.

11.   Where in the brain are the smells perceived?

The olfactory sensory neurons in the olfactory epithelium are directly connected to the olfactory bulb in the brain. The olfactory bulb is connected to a number of higher-order olfactory regions, including the primary olfactory cortex, which is also known as the piriform cortex. Although how smells are perceived is not fully understood, the piriform cortex is likely a key region involved their perception.

12.   Do you think taste is associated only with smell or with loss of tongue sensations?  Is tongue touch sense lost?

Much of changes in taste and flavor of foods may likely be due to alterations in smell. Although I’m not aware of any evidence suggest that tongue sensations are altered, I’m sure that researchers from the Global Consortium for Chemosensory Research and other groups are actively looking into such questions.  

13.   Even the virus impacts only supporting cells, are the neuron functions affected as supporting cells communicate with neurons?

Yes, even if the SARS-CoV-2 virus does not infect the olfactory sensory neurons directly, we do know that functions of these neurons are indeed altered due the wide number of patients with anosmia. The support cells don’t communicate directly with the neurons, and relatively little is known about their function. However, they help maintain ion balance in the nasal mucus and physically they support the sensory neuron dendrites, which contain the olfactory receptors that detect odors. Alterations to either of these supportive functions could affect proper neuron functions and smell.

14.   Are there studies on the pathophysiology on persistent anosmia?

There are relatively few studies, both for persistent anosmia as a result of COVID-19 and for other sources of persistent anosmia (such as after other viral infections). In the non-COVID-19 patients, the persistent anosmia may be due to more permanent damage to the olfactory epithelium, which may even result in the death of olfactory sensory neurons. We think there are basically two types of patients – one that recovers quickly (suggesting that support cell dysfunction is acutely preventing smell) and one that recovers slowly (suggesting that ongoing support cell dysfunction leads to sensory neuron death).

15.   Do you think the loss of smell in COVID19 may be related to the loss of smell reported in some dementia in aging?

This is an interesting question. Although it is true that olfactory impairments have been reported for a number of neurodegenerative diseases, it is unclear whether the underlying mechanisms are similar. However, COVID-19-associated anosmia does appear to resolve relatively quickly and can likely be explained by peripheral changes in the olfactory epithelium. In contrast, the anosmia reported in neurodegenerative disorders is more likely to be due to central alterations within the brain.

16.   Might the infection of olfactory support cells ultimately affect neurons, perhaps vía effects of ex oso al transfer?

We do know that the infection of supportive cells does indeed ultimately affect neurons given the high rates of anosmia. However, anosmia could result from a number of indirect/secondary effects on the neurons, rather than subsequent direct infection. I am not aware of any reports of the exosomal transfer of the SARS-CoV-2 viral particles. Nevertheless, even in the brain, one could imagine that the local perfusion of inflammatory cytokines from the infected vascular supportive cells could indirectly affect neuron function.

17.   Would COVID affect the sense of smell in elderlies more than younger patients?

Although the risk for severe illness with COVID-19 increases with age, I am not aware of any studies suggesting that anosmia is worse depending on age. If anything, the median age of COVID-19 patients with smell loss is lower than that of patients with more severe symptoms. Further research is definitely needed to see which symptoms are age-dependent, and why.

18.   What is the relation of anosmia in Covid with the incubation of the virus?

I am not aware of whether this has been studied, as it would require longitudinal monitoring of both olfactory symptoms as well as viral loads. It is, however, known that anosmia can be one of the first or only symptoms reported for some patients. 

19.   What is the role of the olfactory support cells in the sense of smell? What do your findings suggest about the importance of these cells?

Great questions. One thing that this research has made clear to us is just how little we know about the function of these supportive cells in the olfactory epithelium. One type of supportive cell that we have been focusing on are sustentacular cells. The general thought is that they are important for maintaining ion balances in the nasal mucus so that the sensory neurons can signal properly. Additionally, they also appear to have a structural role, and they help wrap around and support the olfactory sensory neuron dendrites, whose cilia face the nasal mucus and contain the olfactory receptors necessary for detecting odorants. It is still unclear which of these functions may be disrupted during COVID-19, but it is definitely true that to date the roles they play in normal olfactory function have been largely underappreciated.

20.   What is the likelihood of coronavirus infection having an adverse effect on neurobehavioral development during the embryonic/fetal periods of development?

The risk of passing the SARS-CoV-2 virus to a fetus appears to be low, and there have not been any reports of fetal malformations.

21.   I’d like to ask to Mr. David Brann. Do you think anosmia could be considered as one of the important cardinal signs to diagnose a patient with Covid-19 in clinical settings?

Yes, anosmia has already been shown to be one of the most predictive symptoms, and it appears to be more specific than other symptoms like fever. Therefore, recent changes in the sense of smell (with or without the other CDC/WHO symptoms) could likely indicate that someone has COVID-19. However, the most definitely way to evaluate the presence of the SARS-CoV-2 is via the molecular RNA tests.

22.   Are there underlying reasons why men are more susceptible to COVID? Do men and women exhibit symptoms differently, such as loss of smell?

There are a number of biological, behavioral, and social factors that may make men more at risking of dying from COVID-19. However, there is less of an effect of sex on getting COVID-19. Although preexisting health conditions, including those that differ based on sex, can affect COVID-19 symptoms, I am unaware of any evidence suggestions that the loss of smell disproportionately affects one based on sex.

23.   When discussing about a vaccine, in your research study, do you see a possibility of using the olfactory system of creating a vaccine?

Not at the moment. Of the 160+ vaccines in development, some of them are considering intranasal delivery strategies, but like the more-common intramuscular vaccines, the goal of them is still to stimulate the immune system. That said, monitoring the effects of these vaccines on infection in the olfactory system and subsequent rates of anosmia would likely be fruitful given the high rates of anosmia in COVID-19.

24.   Previous pandemics resulted in an increase in "hyperkinesis" in children and "Parkinson's disease in adults.  Have you considered this age-related effect?

It is likely too early to tell if SARS-CoV-2 infection could increase the risks for Viral Parkinsonism. However, the viruses that have been linked with increased risk for Parkinson’s are typically not coronaviruses. Additionally, many of these viruses have been shown to have higher rates of viral encephalitis, which appears to be a relatively rare symptom in COVID-19.

25.   Does anosmia affect all ages similarly? And are there differences in the ACE2 expression in olfactory epithelium and brain depending on age?

Although the risk for severe illness with COVID-19 increases with age, I am not aware of any studies suggesting that anosmia is worse depending on age. If anything, the median age of COVID-19 patients with smell loss is lower than that of patients with more severe symptoms. Further research is definitely needed to see which symptoms are age-dependent, and why. There are also conflicting reports on the effect of age (and other preexisting health conditions) on ACE2 expression. In general, the expression levels of ACE2 in the olfactory and nasal epithelia are relatively high compared to other regions like the lungs. In the brain, there is no solid evidence for ACE2 expression in neurons, and in the vascular cells that do express ACE2, no evidence to date that its expression changes with age. ACE2 expression may also be regulated by the immune system, and aspects of the immune response to SARS-CoV-2 infection also changes with age.

26.   Is there data about if the lack of taste is also related to the nervous system?

Alterations in the sense of taste in COVID-19 could be due to the loss of smell, or they could be the result of COVID-19 directly targeting the taste system, perhaps at the level of the taste buds in the tongue or at the sensory ganglion. Further research is needed to understand how COVID-19 leads to alterations in the sense of taste.

27.   Is there research on changes in the representation of Olfactory signals in OSN, Glomeruli and OB change pre and post COVID infection?

Good question. I am not currently aware of any research, in either model organisms like mice (where most of the OSN/glomerular imaging has been performed) or in humans (via functional imaging studies). Structural imaging in humans (e.g. CT and MRI) have identified relatively little alterations in the OB of patients with COVID-19-associated anosmia. One thing that is interesting to note is that there are now reports of patients with only partial recovery of their sense of smell or smell distortions (parosmias). It will be interesting to see whether such parosmias are attributed to alterations at the periphery in olfactory receptor expression patterns and OSN signaling, or from central changes in either the OB or piriform cortex.

28.   Any hypothesis for how infection of the supportive cells produces anosmia?

One type of supportive cell that we have been focusing on are sustentacular cells. The general thought is that they are important for maintaining ion balances in the nasal mucus so that the sensory neurons can signal properly. Additionally, they also appear to have a structural role, and they help wrap around and support the olfactory sensory neuron dendrites, whose cilia face the nasal mucus and contain the olfactory receptors necessary for detecting odorants. Additionally, damage to sustentacular cells could also release cytokines that could cause local inflammatory responses. Further research, especially in model organisms, is necessary to help differentiate between these possible mechanisms.

29.   Is there data about possible neuroinflammatory mechanism for smell effect of SARS-COV-2 virus?

Current data have suggested that COVID-19 patients can have anosmia without widespread nasal obstruction or inflammation. However, there is also the possibility that anosmia could result from more localized inflammation, which is consistent with clinical reports that have found some inflammation in the olfactory clefts. Infection of supportive cells in the olfactory epithelium, for example, could cause the release of inflammatory cytokines.

30.   Is there an opportunity to study Neurogenesis in the Olfactory system in humans post COVID-19 infection?

Neurogenesis has been difficult to study in humans, and there is relatively little work with human nasal biopsy samples, and even less with the human olfactory bulb. There could be opportunities to evaluate markers for neurogenesis in the olfactory systems of post-mortem samples.

31.   Does the treatment of anosmia in Covid the same as the common flu anosmia?

In both cases, there are unfortunately relatively few treatments options for patients where the loss of smell doesn’t recover after the viral infection. Current treatments for non-COVID-19 cases of anosmia include steroids to decrease inflammation; in COVID-19, many patients have anosmia without significant inflammation, suggesting that steroids may be less effective. It has been suggested that smell training could help the recovery of patients with persistent anosmia, but further research and clinical studies on treatment options for anosmia is needed—especially for patients with long-lasting symptoms.

32.   What are your thoughts on COVID-19 and the future prevalence of Parkinson’s disease? One of the major triggers for PD is having viral infections throughout one’s life, would you say that COVID can be also counted as a trigger of PD?

It is likely too early to tell if SARS-CoV-2 infection could increase the risks for Viral Parkinsonism. However, the viruses that have been linked with increased risk for Parkinson’s are typically not coronaviruses. Additionally, many of these viruses have been shown to have higher rates of viral encephalitis, which appears to be a relatively rare symptom in COVID-19.

33.   Is there research on changes in the representation of Olfactory signals in OSN, Glomeruli and OB change pre and post COVID infection?

Good question. I am not currently aware of any research, in either model organisms like mice (where most of the OSN/glomerular imaging has been performed) or in humans (via functional imaging studies). Structural imaging in humans (e.g. CT and MRI) have identified relatively little alterations in the OB of patients with COVID-19-associated anosmia. One thing that is interesting to note is that there are now reports of patients with only partial recovery of their sense of smell or smell distortions (parosmias). It will be interesting to see whether such parosmias are attributed to alterations at the periphery in olfactory receptor expression patterns and OSN signaling, or from central changes in either the OB or piriform cortex.

34.   Any thoughts on the inflammatory nature of the COVID-19 infection relating to anosmia.  Thinking of the ACE-2 vasoconstriction effects

Although SARS-CoV-2 uses ACE2 for cell entry, it is still unclear to what extent the virus actually interferes with the renin-angiotensin system. At least for anosmia, many patients have reported the loss of smell in the absence of widespread nasal inflammation. However, one possibility is that more localized inflammation (e.g. within the olfactory cleft), could also contribute to anosmia.   

35.   In Spanish flu survivors, many developed Parkinson’s disease and an early symptom of Parkinson’s disease is anosmia. Does this raise concern for Covid-19 survivors’ risk of neurodegenerative disease?

It is likely too early to tell if SARS-CoV-2 infection could increase the risks for Viral Parkinsonism. However, the viruses that have been linked with increased risk for Parkinson’s, such as the H1N1 influenza virus that caused the 1918 pandemic, are typically not coronaviruses. Additionally, many of these viruses have been shown to have higher rates of viral encephalitis, which appears to be a relatively rare symptom in COVID-19.

36.   Is there an opportunity to study Neurogenesis in the Olfactory system in humans post COVID-19 infection?

Neurogenesis has been difficult to study in humans, and there is relatively little work with human nasal biopsy samples, and even less with the human olfactory bulb. There could be opportunities to evaluate markers for neurogenesis in the olfactory systems of post-mortem samples.

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Andrew Chen

Dr. Porteous' responses:

1.       I would like to have thoughts on potential covid-19 triggered endemic of Neuropsychiatric disorders, akin to what happened post Spanish flu (encephalitis lethargica)?

Too early to say, but we are seeing evidence of PTSD-like responses and phobia’s over easing of lockdown. Long term follow up is needed. There are worries that reduced contact between babies and very young children and e.g. grandparents will be harmful, but that is probably balanced by more contact with both parents. Young children seem to be more resilient that older teenagers and young adults.  There is evidence too that those with autism and learning difficulties have had a tough time because of reductions in support and carer contact. Facemasks are problematic both ways.

2.       What is the older health care system like in Scotland/UK? It seems surprising that the younger are more affected in terms of isolation, depression, etc than older. For example here in Canada, some long-term care homes were not allowed to have visitors, may not have had technical support to talk to family remotely, and as I understand, there were very high levels of isolation, some refusing to eat due to depression, and have died as a consequence.

 Good question. Our survey is biased towards those who are online so is not capturing the impact on the more frail living in care homes. On looking more closely at the data, we do see an upturn on loneliness/isolation in the 80+ group. What struck as most however what the strong effect on younger adults and this continues into older teens.  This is an important group who will be most impacted as they move from education into occupation and self-sufficiency.

  3.       Have you looked at the disparities in those with existing neurological disorders or disabilities? I work in a neurorehab clinic and have been seeing patients virtually, they report feeling scared, lonely, and have limited access to resources if they live alone/geographical location. Just wondering if any of your data has captured the experiences of this particular population.

No we haven’t but the reports of high levels of delirium in those with COVID is noteworthy. Delirium as a component of trauma and neurological damage is under recognized. Online consultations have been a life line in many contexts and I expect that many healthcare systems will place increasing emphasis on telemedicine, but you are right to highlight that fact that person-to-person contact is core to doctor-to-patient relations and rehabilitation particularly in the vulnerable and frail. We have to recognize and preserve this, particularly for older patients. Trials of that compare personal, virtual (flat screen) and VR would be a good idea. 

4.       Why do more males have COVID?

Let’s be honest, we are the weaker sex. Think of man flu? Think too of what most women cope with as part of monthly life, child bearing and menopause that men don’t. But seriously, there are probably other reasons, including a higher risk of chronic workplace exposure, lower intrinsic compliance with mitigation measures (such as hand washing) and physiologically, from hormone related immune response mechanisms. There is a lot still to tease out.    

5.       What do you think is the long-term mental health effect of the young people in the future? Are we looking at increase psychological disorders later in life? Would the effects be permanent?

We know that early life events are important triggers for later onset psychiatric problems that can be long-standing so we need to take a long view. Balanced against that, we have resilience and so the efforts of parents, teachers, friends, community to rally round and help each other to bounce back will be important. So too will community, national and international leadership. One major life changing event to life through is one thing, but if through negligence or lack of forward planning we are hit by a second wave or new infection in the near term, that could be very damaging from a psychological/psychiatric perspective.  

6.       Your comment about "Share feelings with others" Do you recommend that for high school teachers at the start of the year, or should we offer something apart from the stresses of COVID-19?

Our TeenCovidLife survey was designed to give young people a voice and to give teachers a ‘heads up’ about the impacts. We see this as a process and an opportunity. The more children, parents, friends and teachers know that these are issues to be shared and lived through together the better.  A good opener will be along the lines of ‘I don’t know about you, but I have found this (COVID) really difficult at times. Example. Etc. What about you?

7.       Has there been an effect on dietary habits due to lockdown? More vegan or more non-vegan?

In the UK, things seemed to stat well, with lots of on line ideas for eating well. The stores ram out of flour and yeast as people took to baking bread, but also cakes (not so good). Veg consumption went up and meet down. Sadly, as lockdown continued, bad and worse habits have returned. As food outlets opened, they were take-away only and more junk that nutritious. So sadly, obesity is on the rise again. It is a very common risk factor for COVID. The UK government is trying to tackle this, through a number of measures from banning junk food advertising before 9pm to encouraging cycling with more cycle lanes and voucher to get old bikes serviced and back on the road (as France did early on).

8.       Did your surveys include disabled or immunocompromised people? It seems that able bodied people brush Covid off as something that only seriously affects the disabled and immunocompromised.

There are no exclusions to participation, but it is all online (PC, laptop or smart phone). Yes we do ask questions about general health, whether they or someone in their household is self-isolating or shielding because of specific risk factors. The numbers are modest. We also ask questions about understanding, believing in and complying with the guidance on mitigation (hand washing, social/physical distancing etc). The disastrous consequences of COVID parties should be published more widely. Legal enforcement of mitigation measures is problematic. As an alternative to fines however, a spell of unpaid frontline work experience might do the trick on compliance. 

 9.       What are your thoughts on young people adjusting their sleep schedules to a more natural rhythm without the usual constraints on time and school start times/ outside activities.

It is an interesting idea and there is a strong body of evidence to suggest that for teenagers a later start to the school day might actually pay off. As schools return, staggered starts might work. The big problem then is for working parents whose caring responsibilities will be stretched and work time compressed.

10.   Do you think there will be a mental health cohort effect in adolescents growing up during this? Or will rates of mental illness be similar to other cohorts (e.g. people getting mentally ill are people who would have become ill due to different stressors, just at different times)

It’s something we need to watch out for and monitor.

 11.   Hello, did you observe prolonged cognitive decline in persons that had COVID-19 in relation of non-infected persons?

We have not looked at that yet, but others are. We have however done a lot of work on cognitive ageing pre-COVID and we will be looking at this now that that we have the unique opportunity of pre-COVID trajectories now linked or linkable to COVID and post-COVID medical records and the ability to offer cognitive tests as part of our volunteer recontact capability.

12.   What is the likelihood of coronavirus infection having an adverse effect on neurobehavioral development during the embryonic/fetal periods of development?

I don’t know, but I do know that this is being looked at by others.

13.   Is there any organization (private or public) that is tracking all indicators data of mental health associated with covid-19 pandemic?

There are a couple of initiatives to collate all of this in this for UK studies, e.g. by the Mental Health research charity MQ https://www.mqmentalhealth.org/news-blog/tag/coronavirus-covid-19 and Daisy Fancourt https://www.ucl.ac.uk/news/2020/mar/new-study-psychological-and-social-effects-covid-19

 14.   To Prof Porteous, how do you believe these findings on mental health will be used in the long-term? Do we believe this will be something that will affect our society negatively in the grand scheme of things?

It could if a) we don’t act to recognize and respond or b) experience another wave or new virus without adequate preparation. The reason that depression is second only to heart disease on DALYs is that it is recurrent and debilitating in many ways, likewise anxiety, PTSD and other conditions. If we just go back to the status quo, propping up traditional industries, ‘wealth’ metrics and ways of life, rather than people and qualities of life, we will have missed a big trick and a once in a generation chance for a rethink and renew.    

15.   Do you have any comments or on-going studies of effects of the pandemic on health care workers?

Our focus has been on the general population, but other are focusing on health care workers and watch this space for more on the UK GOV response to COVID-19 population impact studies.

16.   Are impacts in mental health caused by COVID transient?  will you predict life-long impacts in their mental health in particular young adults even after COVID is over, hopefully, in future ?

 Difficult to say at this stage. Longitudinal studies are needed. We are on it, as are others.

17.   Are there any datasets available to researchers (e.g. smell and COVID or the public heath surveys of Scotland)?

 The C-19 app (Kings College London / Zoe collaboration) is tracking signs and symptoms in ~4 million in the UK. https://covid.joinzoe.com/

18.   In Spanish flu survivors, many developed Parkinson’s disease and an early symptom of Parkinson’s disease is anosmia. Does this raise concern for Covid-19 survivors’ risk of neurodegenerative disease?

Long term follow up is needed. Very important though to distinguish cause from effect, so pre-COVID data is important. Are these symptoms spotted because we are looking hard and they were there pre-COVID or are they a direct or indirect consequence of infection?

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