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Alzheimer's disease and coronavirus: some common threads
Lane Simonian
Posted: Friday, March 27, 2020 10:46 PM
Joined: 12/12/2011
Posts: 5137

Ed posted information that loss of smell is sometimes a symptom of a coronavirus infection.  Loss of smell can also be a sign of impending Alzheimer's disease.  Loss of smell is often one of the first casualties of oxidative stress.

Chloroquine (and hydroxychlorquine) has been suggested as a potential treatment for Alzheimer's disease.  Chloroquine indirectly limits oxidative stress and subsequent inflammation as a sigma-1 agonist.

But hdyroxychlroquine failed to treat Alzheimer's disease and it probably will also fail to treat infections due to the coronavirus.

Anavex 2-73 is a sigma-1 agonist currently being studied for Alzheimer's disease.  It may do better than hydroxychlorquine because it is also a direct antioxidant.

Eugenol may have some affect against viruses both by limiting oxidation and inflammation and by damaging the viruses themselves.

Eugenol (found in various essential oils such as clove, rosemary, cinnamon, and bay laurel) may help in the treatment of Alzheimer's disease because it has antioxidant properties that then limit inflammation.

Panax ginseng contains multipe compounds that are antioxidants.  Like eugenol, these compounds may help in the treatment of various viral infections.

Panax ginseng has also shown promise in the treatment of Alzheimer's disease.

Viruses and various other factors (at times through the nose) provoke oxidative stress leading to inflammation leading to further oxidation.  Compounds that interfere with these processes have the best chance to treat both viral infections and Alzheimer's disease.

Lane Simonian
Posted: Friday, April 24, 2020 10:13 AM
Joined: 12/12/2011
Posts: 5137

Some research indicates that cytokine storms (producing massive inflammation) are responsible for some of the mortality from the coronavirus.  This is one of the best explanations that I have seen so far as to the nature of cytokine storms.

"Until now, numerous studies have indicated cytokine storm and oxidative stress are highly assoication with the pathological process when getting infrected with these viruses.  Although cytokine storm and oxidative stress probably try to eliminate these pathogens, they seem to generate multi-organ damage resulting in lethal clinical symptoms such as extensive pulmonary oedema, alveolar and other tissue haemorrhage, and acute respiratory distress syndrome, etc.  Moreover when inflammation and oxidative stress damage tissue and organs, healing occurs with fibrosis, aggravating persistent multiple organ dysfunction.  Therefore, timely elimination of these mass of cytokines and oxidative stress would presumably protect normal organs from the damaging effects of pathogen infection."

In a way, Alzheimer's disease may be considered a slow rolling cytokine storm (although many things besides chronic viruses can initiate this "storm").

"We argue that understanding cytokine storms in their various degrees of acuteness, severity and persistence is essential in order to grasp the pathophysiology of many diseases, and thus the basis of newer therapeutic approaches to treating them. This particularly applies to the neurodegenerative diseases."

In viral diseases and in Alzheimer's disease, there is a triggering agent.  In viral diseases, the triggering agent is easy to identify it is the virus and it can act in a quick and overwhelming fashion.  In Alzheimer's disease, there are likely multiple triggering agents that slowly act over many years.  In both cases if you can limit or eliminate the effects of the triggering agent or agents early (before they lead to severe oxidation and inflammation), you can limit or prevent organ damage. But once the disease has taken hold a different approach is likely needed.

Indeed, the key to treating Alzheimer's disease as it may be in many viral diseases is to break the cycle of oxidation and inflammation.  

Lane Simonian
Posted: Thursday, April 30, 2020 10:12 AM
Joined: 12/12/2011
Posts: 5137

Here is another restatement of what causes a large amount of the damage in viral infections:

It is...well known that the majority of viral-induced tissue damage and discomfort are mainly caused by an inflammatory cytokine storm and oxidative stress rather than by virus itself.  Studies have shown that surpressing the cytokine storm and reduing oxidative stress can significantly alleviate the symptoms of influenza and other severe viral infection diseases...

Importanly, excessive inflammation reaction can also induce acute oxidative stress.  Together, both cytokine storm and oxidative stress promote each other...

The same is also true for Alzheimer's disease:

Oxidative stress is intimately associated with neuroinflammation, and a vicious circle has been found to connect oxidative stress and inflammation in AD

Like viruses, amyloid causes little to no damage by itself but it can cause damage through oxidation and inflammation.  But so too can dozens of other factors.

Another critical point is that through DNA damage and tissue damage, oxidation drives inflammation which leads to more oxidation.  Anti-inflammatories only slow down this process to a small degree whereas certain antioxidants cannot only grind this process to a halt but can to a certain degree reverse the damage that has already been done.  That is why certain antioxidants have led to small improvements in mild to moderate Alzheimer's disease that were sustained over time.

Lane Simonian
Posted: Monday, May 4, 2020 11:58 PM
Joined: 12/12/2011
Posts: 5137

Of 200 herbs studied for the treatment of coronaviruses, the two that appear to be the most effective were first Lycoris radiata (red spider lilly) and second Artemesia annua (from which the anti-malarial drug artemisinin is derived).  So I looked up information on both for Alzheimer's disease:

Lycoris radiata (L'Her.) Herb. (L. radiata) was traditionally used as a folk medicine in China for treatment of Alzheimer's disease. However, the specific component responsible for its considerable toxicity remained unclear thus restricting its clinical trials.

Artemisinin, also called qinghaosu, is originally derived from the sweet wormwood plant (Artemisia annua), which is used in traditional Chinese medicine. Artemisinin and its derivatives (artemisinins) have been widely used for many years as anti-malarial agents, with few adverse side effects. Interestingly, evidence has recently shown that artemisinins might have a therapeutic value for several other diseases beyond malaria, including cancers, inflammatory diseases, and autoimmune disorders. Neurodegeneration is a challenging age-associated neurological disorder characterized by deterioration of neuronal structures as well as functions, whereas neuroinflammation has been considered to be an underlying factor in the development of various neurodegenerative disorders, including Alzheimer’s disease. Recently discovered properties of artemisinins suggested that they might be used to treat neurodegenerative disorders by decreasing oxidation, inflammation, and amyloid beta protein (Aβ). In this review, we will introduce artemisinins and highlight the possible mechanisms of their neuroprotective activities, suggesting that artemisinins might have therapeutic potential in neurodegenerative disorders.

You have to love plants, or at least some of them.

A thank you to those who have thanked me on other threads in recent days.  I don't always get things right and I have not always given the best advice, but I have tried very hard to be both right and helpful.

Posted: Thursday, May 7, 2020 1:42 PM
Joined: 11/13/2014
Posts: 2366

Article about aluminum and early onset or younger adults getting alz and dementia. It's not really just younger adults.either. 

Robert Kennedy JR..(another hero of mine)


Lane Simonian
Posted: Thursday, May 7, 2020 3:58 PM
Joined: 12/12/2011
Posts: 5137

Thank you for posting this very good article, Deb.  I do believe a variety of environmental toxins can spead the onset of Alzheimer's disease, either with or without genetic factors.

Robert Kennedy Jr. is one of my heroes as well.

Lane Simonian
Posted: Tuesday, May 26, 2020 7:34 PM
Joined: 12/12/2011
Posts: 5137

This is another fascinating common thread: having one or two copies of the APOE4 gene increases the risk for coronavirus just as it does Alzheimer's disease.

The APOE ε4 gene variant that puts people at a greater risk of developing Alzheimer’s disease also has a link to COVID-19. According to a study published today (May 26) in The Journals of Gerontology, Series A, carrying two copies of the variant, often called APOE4, makes people twice as likely to develop a severe form of the disease, which is caused by the SARS-CoV-2 coronavirus currently spreading around the world.

The APOE4 gene increases lipid rafts (consisting of cholesterol and fatty acids) which amplifies a variety of factors that result in oxidation and inflammation and a variety of diseases. 

One of the key mediators of these processes is Nuclear factor KappaB:

Apolipoprotein E4 Enhances Brain Inflammation by Modulation of the NF-kappaB Signaling Cascade

Activation of NF-kappaB by the Full-Length Nucleocapsid Protein of the SARS Coronavirus

Nuclear Factor-Kappa B and Alzheimer Disease, Unifying Genetic and Environmental Risk Factors from Cell to Humans

Lane Simonian
Posted: Wednesday, June 10, 2020 10:35 AM
Joined: 12/12/2011
Posts: 5137

In a way, it is nice to see some scientists beginning to make the connection between the coronavirus and Alzheimer's disease:

Studying connection between Alzheimer’s Disease and coronavirus

The connection between Alzheimer’s Disease and coronavirus is apparent, but not yet understood said a doctor who is helping lead a study to find a cure for Alzheimer’s. Indiana University is one of the testing sites for that study.

“This is a dosease, which we see from COVID, how vulnerable people with Alzheimer’s Disease are to communicable diseases,” said Dr. Jeffrey L. Cummings, Research Professor, Department of Brain Health at the University of Nevada at Las Vegas.

“For reasons that are still to be determined we see that almost a third of all the deaths from COVID are nursing home residents and most of those residents have Alzheimer’s Disease,” he said. “So, there is some vulnerable link between Alzheimer’s Disease and COVID that we have yet to fully understand. But, what we see is the tremendous vulnerability that Alzheimer’s Disease has when it comes to COVID.”

Certainly crowded conditions play a role, but the question is are those with Alzheimer's disease more vulnerable to the coronavirus and if so why.

Part of the problem may be lower levels of T-cells in people with Alzheimer's disease which may make it harder for them to fight off the infection.

Another problem is that the two diseases may share a common etiology: widespread oxidative damage and  inflammation.

A novel functional beverage for COVID-19 and other conditions: Hypothesis and preliminary data, increased blood flow, and wound healing

COVID-19 is caused by a viral infection, and can be a lethal disease to the immunocompromised. HydroShot is a popular functional health beverage that is infused with molecular hydrogen, and contains the nitric-oxide-producing amino acid citrulline. Numerous pre-clinical and clinical studies have demonstrated that the gaseous-signaling molecules, molecular hydrogen and nitric oxide, have anti-oxidant, anti-inflammatory, and immuno-modulating benefits. Although nitric oxide can directly kill pathogens, it is critical for immune function, can inhibit viral replication, and can also induce lethal cellular injury under stressed conditions. In contrast, molecular hydrogen has a very high safety profile and helps regulate nitric oxide production, metabolism, and attenuates its harmful effects. Both of these molecules are being used separately in clinical trials for COVID-19 patients...

H2 and NO work together to suppress COVID-19-induced oxidative stress and inflammation, which helps to prevent multiple organ failure and death.

Molecular hydrogen and nitric oxide combination

Nitric oxide, as a reactive free radical, encourages either cell survival or cell death depending on its concentration, location, and timing of production. Importantly, molecular hydrogen regulates nitric oxide (NO•) levels via both reducing excessive production (e.g. suppressing iNOS activity) and also increasing production (e.g. enhancing eNOS activity) [5]. Therefore, NO• regulation is critical to potentiate its beneficial therapeutic effects and mitigate its harmful effects. NO• reacts nearly instantaneously with superoxide (O2•-) to form pernicious peroxynitrite (ONOO-), which is an extremely oxidative and cytotoxic molecule [25]. The reaction with O2•- directly lowers the availability of circulating NO•, which further exacerbates the diseased condition [25]. The radicals, O2•- and NO•, have important beneficial roles in the immune system including killing pathogens, inhibiting their replication, and regulating the inflammatory response. However, under stressful conditions, such as with COVID-19 and its progression to pneumonia, multi-organ failure, and other sequelae, these molecules lose their critical regulation and contribute to the etiology and pathology of these diseases forming both ONOO- and the extremely toxic hydroxyl radical (•OH) [25]. Molecular hydrogen has been demonstrated to favorably regulate the production of both O2•- and NO• by influencing NADPH oxidase, and the NOS enzymes (iNOS, eNOS and nNOS) [5]. Additionally, H2 can effectively reduce the toxic hydroxyl and peroxynitrite oxidants [4]. Furthermore, combination therapy of NO• and H2 demonstrated a synergistic effect in an acute lung-injury model such as what can occur with COVID-19. The treatment significantly attenuated lung neutrophil recruitment, inflammation, and apoptosis induced by LPS and polymicrobial sepsis [26]. Moreover, H2 prevented NO•-induced damage as evidenced by the elimination of nitrotyrosine levels seen with NO• therapy alone [26]. This adds credence to the concept that oral ingestion of HydroShot, a hydrogen-infused functional beverage containing NO•-producing citrulline, may provide significant benefits to the immune system. 

Molecular hydrogen also has been suggested as a treatment for Alzheimer's disease:

The role of hydrogen in Alzheimer′s disease

Alzheimer’s disease is one of the most common neurodegenerative diseases in the elderly. It is often manifested as learning and memory impairment, cognitive function decline, normal social and emotional disorders. However, for this high-risk common disease, there is currently no effective treatment, which has plagued many clinicians. As a new type of medical therapeutic gas, hydrogen has attracted much attention recently. As a recognized reducing gas, hydrogen has shown great anti-oxidative stress and anti-inflammatory effect in many cerebral disease models. It can ameliorate neuronal damage, maintain the number of neurons, prolong the lifespan of neurons, and ultimately inhibit disease progression. Therefore, the role and mechanism of hydrogen in the pathological process of Alzheimer’s disease will be discussed in this paper.

If oxidative stress is at the heart of both the novel coronavirus and Alzheimer's disease then there may be a shared treatment for both.

Lane Simonian
Posted: Thursday, June 25, 2020 9:37 AM
Joined: 12/12/2011
Posts: 5137

I sadly figured a headline like this was going to appear sooner or later.

Neurologist: COVID-19 can cause memory loss, Alzheimer’s


Dr. Fotuhi’s findings have been published in the Journal of Alzheimer’s Disease.


Fotuhi found COVID causes brain damage in three stages: first, patients have difficulty with only smell and taste (more than 80 percent of the time symptoms resolve within a few weeks without interventions); second, patients have inflammation in the blood vessels that result in blood clots (those that develop in the brain can cause small or large strokes); and third, patients have damage to the blood vessels in the brain (blood vessels provide oxygen and nutrients to the brain) that cause blood and chemicals to leak into the brain, killing brain cells and causing seizures, confusion, or bleeds in the brain. This can lead to memory loss, confusion, cognitive impairments, and Alzheimer’s disease later in life. 

If true, the coronavirus would join a relatively long list of viral and bacterial infections tentatively linked to an increased risk of Alzheimer's disease.

The two main receptor types which can trigger Alzheimer's disease are g protein-coupled receptors and receptor tyrosine kinases.  The coronavirus over-activates a particular kind of g protein-coupled receptor:  the angiotensin II receptor.

Anti-hypertensive Angiotensin II receptor blockers associated to mitigation of disease severity in elderly COVID-19 patients.

In some cases, angiotensin II receptor antagonists can help reduce the risk of Alzheimer's disease.,and%2For%20amyloid%20%CE%B2%20deposition.

Posted: Thursday, June 25, 2020 9:49 AM
Joined: 5/22/2020
Posts: 9

I think it it’s very unlikely, that a covid infection leads to one of the stage 3 symptoms, and It’s even more unlikely it can lead to Alzheimer’s.
Lane Simonian
Posted: Thursday, June 25, 2020 9:52 AM
Joined: 12/12/2011
Posts: 5137

Back for a moment to T cells.  T cells appear to be important for clearing the coronavirus.

And probably a key finding:

"Additionally, upon discovering that COVID-19 patients had significantly higher concentrations of cytokines, The authors suggested that rather than directly attacking T cells, the COVID-19 virus triggers a cytokine storm, which then acts to drive down T cell numbers.”

In Alzheimer's disease, low T cells levels may inhibit the removal of amyloid oliogmers, which at least in the case with those who have the ApoE4 gene or genes may accelerate the progression of Alzheimer's disease early on.

Low T cell levels can also inhibit the removal of cancer cells.

Viruses, amyloid, and cancer cells find a way to avoid detection and removal by disabling T cells via peroxynitrite.  In theory, the same peroxynitrite scavengers that help in the treatment of Alzheimer's disease could also help in the treatment of the coronavirus and cancer.

Lane Simonian
Posted: Thursday, June 25, 2020 9:34 PM
Joined: 12/12/2011
Posts: 5137

Today appears to be my lucky research day:

One new drug may treat both Covid-19 and Alzheimer’s

Israeli-born Harvard professor’s investigational therapy suppresses immune system’s overproduction of proteins that trigger inflammation.

A novel Alzheimer’s disease treatment now in advanced Phase 3 clinical trials could also prove effective in treating lung inflammation caused by Covid-19.

The investigational therapy, ALZT-OP1, suppresses the immune system’s production of cytokines — proteins that trigger inflammation in a natural response to infection...

A “cytokine storm” caused by an overzealous immune response plays a role in neuroinflammatory diseases such as Alzheimer’s, and in infectious diseases such as Covid-19 and influenza...

ALZT-OP1 is a proprietary mixture of a bit of ibuprofen (to treat inflammation) and cromolyn, originally an asthma drug.

Cromolyn and low dose ibuprofen both inhibit nuclear factor-kappa Beta.  Such inhibition limits oxidative stress in advance of inflammation.  As far as I know, though, neither scavenge nor reverse the damage done to the lungs and brain by peroxynitrite.  There are a number of other compounds that do all three.  I would be surprised that if a successful treatment for this novel coronavirus is found it would not also help in the treatment of Alzheimer's disease--similar disease mechanisms; similar pathways; and to a certain degree similar damage.

Lane Simonian
Posted: Saturday, June 27, 2020 10:09 AM
Joined: 12/12/2011
Posts: 5137

I was watching an interesting program on bats and the coronavirus last night and one of the questions raised is why aren't bats affected/infected by the coronavirus like humans.  Here may be part of the answer.

The secret to bats' immunity

Bats live very long and host numerous viruses, such as Ebola virus, Nipah virus, and severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) coronaviruses, that are extremely harmful when they infect humans and other animals. Researchers at Duke-NUS Medical School and colleagues wanted to find out how bats can harbour so many of these pathogens without suffering from diseases.

The key, they found, is in the bat's ability to limit inflammation. Bats do not react to infection with the typical inflammatory response that often leads to pathological damage. In humans, while the inflammatory response helps fight infection when properly controlled, it has also been shown to contribute to the damage caused by infectious diseases, as well as to aging and age-related diseases when it goes into overdrive.

The researchers found that the inflammation sensor that normally triggers the body's response to fight off stress and infection, a protein called NLRP3, barely reacts in bats compared to humans and mice, even in the presence of high viral loads.

"Bats' natural ability to dampen inflammation caused by stress and infection may be a key mechanism underlying their long lifespans and unique viral reservoir status," said Dr Matae Ahn, first author of the study and an MD-PhD candidate of the Emerging Infectious Diseases (EID) Programme at Duke-NUS Medical School.

The researchers compared the responses of immune cells from bats, mice and humans to three different RNA viruses -- influenza A virus, MERS coronavirus, and Melaka virus. The inflammation mediated by NLRP3 was significantly reduced in bats compared to mice and humans.

Digging further, they found that 'transcriptional priming', a key step in the process to make NLRP3 proteins, was reduced in bats compared with mice and humans. They also found unique variants of NLRP3 only present in bats that render the proteins less active in bats than in other species. These variations were observed in two very distinct species of bats -- Pteropus alecto, a large fruit bat known as the Black Flying Fox, and Myotis davadii, a tiny vesper bat from China -- indicating that they have been genetically conserved through evolution. Further analysis comparing 10 bat and 17 non-bat mammalian NLRP3 gene sequences confirmed that these adaptations appear to be bat-specific.

What this implies, the researchers explain, is that rather than having a better ability to fight infection, bats have a much higher tolerance for it. The dampening of the inflammatory response actually enables them to survive.

"Bats appear to be capable of limiting excessive or inappropriate virus-induced inflammation, which often leads to severe diseases in other infected animals and people," said Professor Wang Lin-Fa, Director of Duke-NUS' EID Programme and senior author of the study. "Our finding may provide lessons for controlling human infectious diseases by shifting the focus from the traditional specific anti-pathogen approach to the broader anti-disease approach successfully adopted by bats."

Other researchers suggest that the immune response that bats do generate is highly effective against viruses.  So maybe it is a case of a beneficial inmmune response involving part of the bats immune system and a lack of response from the immune system that causes so much damage in humans.

It may go further upstream than this:

Lack of inflammatory gene expression in bats: a unique role for a transcription repressor

In recent years viruses similar to those that appear to cause no overt disease in bats have spilled-over to humans and other species causing serious disease. Since pathology in such diseases is often attributed to an over-active inflammatory response, we tested the hypothesis that bat cells respond to stimulation of their receptors for viral ligands with a strong antiviral response, but unlike in human cells, the inflammatory response is not overtly activated...We measured transcripts for several inflammatory, interferon and interferon stimulated genes using quantitative real-time PCR and observed that human and bat cells both, when stimulated with poly(I:C), contained higher levels of transcripts for interferon beta than unstimulated cells. In contrast, only human cells expressed robust amount of RNA for TNFα, a cell signaling protein involved in systemic inflammation.

The pattern of high levels of TNF alpha, Nuclear Factor-kappa Beta, peroxynitrite, NLPR3 exists in Alzheimer's disease just as they do in coronaviruses.  


Lane Simonian
Posted: Saturday, June 27, 2020 10:31 AM
Joined: 12/12/2011
Posts: 5137

One more for the bats.  In some respects, it appears they evolved better than we did.

Hibernation does not affect memory retention in bats

The hibernated bats performed at the same high level as before hibernation and as the non-hibernated controls. Our data suggest that bats benefit from an as yet unknown neuroprotective mechanism to prevent memory loss in the cold brain.

Antioxidant Defenses in the Brains of Bats during Hibernation

The levels of glutathione (GSH) were higher in Mricketti bats than in Rferrumequinum bats and were significantly elevated in Rferrumequinum bats after torpor. These data suggest that Mricketti bats use mainly antioxidant enzymes and Rferrumequinum bats rely on both enzymes and low molecular weight antioxidants (e.g., glutathione) to avoid oxidative stresses during arousal. Furthermore, Nrf2 and FOXOs play major roles in the regulation of antioxidant defenses in the brains of bats during hibernation. Our study revealed strategies used by bats against oxidative insults during hibernation.

Thank you, bats.

Lane Simonian
Posted: Friday, September 4, 2020 10:11 AM
Joined: 12/12/2011
Posts: 5137

I am sending this message to a group called Survivor Corps which advocates for people suffering long-term health problems related to the coronavirus:

I am saddened by the long-term, debilitating effects that numerous people are suffering from the novel coronavirus.  The following information may be of some use.
First a disclaimer, I am not a doctor nor a scientist.  I do have some background in biology and that background has been strengthened by the sixteen years that I have spent studying Alzheimer's disease.  I have noticed several parallels between Alzheimer's disease and the coronavirus (early loss of smell, the role of angiotensin II receptors, the role of oxidation and inflammation, for instance).  These parallels allow for a better understanding of the coronavirus activated pathways and their consequences for long-haulers.


In Alzheimer's disease, many factors contribute to the overactivation of g protein-coupled receptors and/or tyrosine receptor kinases.  In COVID-19, one factor (the novel coronavirus) leads to the overactivation of one g protein-coupled receptor in particular (the angiotensin II receptor).  The consequence of the overactivation of any of these receptors is the production of superoxide anions.  Superoxide anions can be converted into hydrogen peroxide or combine with inducible nitric oxide to form peroxynitrite.  Through oxidation, these two reactive compounds damage a series of g protein-coupled receptors including those involved in smell, taste, sleep, mood, alertness, and the retrieval of short-term memory.
Oxidants such as peroxynitrite also inhibit the production of endothelial nitric oxide and contribute to atherosclerosis leading to vascular disease (due to vascular constriction and subsequent hypertension).  


In some circumstances, though, peroxynitrite can lead to low blood pressure and sepsis.  

The damage done by oxidation, nitration, and reduced blood flow can damage a series of organs.

Oxidation increases inflammation which further increases oxidation.  Many diseases have been closely linked to peroxynitrite formation including diabetes, glaucoma, tinnitus, heart problems, cancer, and several neurodegenerative diseases including Alzheimer's disease.

Indeed, many of the poorly treated or untreated diseases of our time are likely the consequence of oxidants.  And most likely, many of the long-term side-effects of COVID-19 are also caused by oxidants.  Furthermore, most people with chronic illnesses have fewer t-cells as a result of oxidation and nitration and thus are less likely to "fight off" the virus.

In Alzheimer's disease, hydrogen peroxide levels decrease with the progression of the disease whereas peroxynitrite levels increase.  I think that a similar pattern exists with the coronavirus.  If not, though, some peroxynitrite scavengers are also hydrogen peroxide scavengers.
Certain compounds not only effectively scavenge peroxynitrite they also partially reverse the damage done by oxidation and nitration.  For Alzheimer's disease, these compounds can be found in substances such as panax ginseng (especially heat processed ginseng), essential oils via aromatherapy (especially essential oils high in eugenol such as rosemary, clove, lemon balm, and bay laurel), and medicinal marijuana (low in THC and high in terpenes).  My assumption is that natural products that are successful in treating Alzheimer's disease will also be successful in treating this novel coronavirus and vice versa.  
Hopefully, this information will be of some use to you.  Don't hesitate to follow-up with questions.