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Exercise may protect brain health by keeping insulin, BMI levels low

Exercise may protect brain health by keeping insulin, BMI levels low

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How does exercise protect brain health? New research sheds light. Suhaimi Abdullah/NurPhoto via Getty Images
  • Existing studies show that exercise helps protect brain cells through mechanisms that researchers do not yet fully understand.
  • Researchers know that exercise increases brain glucose metabolism, which correlates with improved brain function.
  • Studies show that exercise affects insulin resistance and has a complex relationship with body mass index (BMI) levels.
  • A new study suggests that exercise plays a role in maintaining insulin and BMI levels, which may help stave off dementia by protecting gray matter volume in the brain.

A new study investigates the mechanisms involved in the relationship between exercise and brain health.

Previous research had shown that larger gray matter volume can help protect against dementia by improving brain function.

The new study shows that insulin resistance and BMI mediate the relationship between larger and smaller brain gray matter volumes (the part of the brain involved in processing information).

The research is published in the April 2022 online issue of Neurology, the medical journal of the American Academy of Neurology.

The corresponding author of the study was Dr. Geraldine Poisnel, of the Inserm Regional Research Center, in Caen, Normandy, France.

The study involved 134 people with an average age of 69 who had no memory problems. The participants filled out a physical activity survey covering the past 12 months. They also had brain scans to measure glucose metabolism and brain volume.

The metabolism of glucose in the brain provides fuel for the brain by generating adenosine 5′-triphosphate (ATP) — a key molecule for maintaining the health of neurons and other cells. ATP is also key for generating neurotransmitters. Reduced glucose metabolism in the brain can be seen in people with dementia.

Gray matter development peaks at age 2–3 years. It begins to decrease afterward in some areas of the brain, but the density of the gray matter increases. From an evolutionary perspective, the higher processing ability of the human brain and its development are due to this increase in density.

In some studies, larger total brain volume, estimated by magnetic resonance imaging (MRI), has a weak correlation with higher intelligence in men and a very weak correlation in women with the ability to do well in intelligence tests.

In contrast, brain tissue deterioration and loss of volume is a significant contributor to lower cognitive ability later in life.

In the new study, researchers included 134 people with an average age of 69 who had no memory problems. The participants filled out a physical activity survey covering the past 12 months. They also had brain scans to measure glucose metabolism and brain volume.

In the new study, researchers gathered formation on cardiovascular risk factors including BMI and insulin levels, as well as cholesterol, blood pressure, and other factors.

The researchers examined the relationship between insulin and cardiovascular disease. The metabolic abnormalities that insulin causes raise the risk of cardiovascular complications, which in turn affect brain function.

Researchers found that insulin and BMI levels did not affect the metabolism of glucose in the brain.

The research demonstrated that the amount of amyloid plaque in the brain that contributes to Alzheimer’s Disease was not affected by exercise.

Medical News Today contacted Dr. Raeanne Moore, associate adjunct professor of psychiatry at UCSD in La Jolla, CA.

Dr. Moore, who was not involved in the study, was asked about the study results. She shared with MNT:

“This study adds to the growing body of research on the positive benefits of staying active on brain health, especially as we age.”

“[T]here is an urgent need to identify markers of cognitive decline,” added Dr. Moore. “Decreasing insulin levels and losing weight are modifiable factors that can be improved with a healthy diet and exercise.”

She added, “It was not surprising that higher physical activity was not associated with how much amyloid plaque people had in their brains. There is growing evidence that vascular risk factors on cognitive function are mediated by the amount of tau pathology in the brain and not an amyloid burden.”

MNT also spoke with Dr. Sheldon Zablow, assistant professor of medicine at University of California San Diego Medical School in La Jolla, CA. Dr. Zablow shared his comments about this study:

“Exercise has often been called food for the brain with many studies showing the benefit of exercise for improving brain health and reducing the risk of dementia.”

“This current research study states that physical activity improves cognitive brain function by reducing BMI and improving insulin metabolism. Improvement in weight control can limit the rate of brain volume loss, a known risk factor for dementia.”

“This study will help physicians reinforce the importance of regular exercise in reducing BMI as a low-cost means of limiting cognitive decline.”

– Dr. Zablow

Dr. Moore’s final remarks were, “The literature clearly demonstrates that cardiovascular risk factors are associated with cognitive decline and risk for Alzheimer’s disease and related dementias.”

“Studies investigating subtle brain changes prior to the development of dementia are critical to optimizing brain health and staving off cognitive decline.”

“Strengths of this study include a sample of cognitively normal older adults and the use of multimodal imaging methods to explore the role of CVD risk factors in the association between physical activity and neuroimaging biomarkers,” said Dr. Moore.

“[T]his methodology can move the field forward by helping to identify important markers of risk for cognitive decline.”

“A limitation to the study was the use of a self-report of physical activity […] which the authors acknowledged as a limitation. Self-report of physical activity is prone to retrospective recall bias, and objective tools to measure physical activity, such as fitness trackers, are more accurate.”

“These findings that insulin and BMI fully mediated the relationship between physical activity and whole-brain gray matter volume — and specifically hippocampal gray matter volume — provide further evidence that targeting these modifiable CVD risk factors could improve brain health.”

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How does COVID-19 affect the brain?

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A recent article in the journal Science outlines what we know about the neurological consequences of SARS-CoV-2 infection. NICOLAS TUCAT/AFP via Getty Images
  • Neurologic complications from COVID-19 are common and can range from decreased mental clarity to stroke.
  • A recent perspective article outlines what we know about these complications so far.
  • The authors explain how prior assumptions that the virus directly affected brain cells have been disproven.
  • Instead, nervous system injury is likely a result of severe inflammation and neurovascular injury.
  • Neurologic insults from SARS-CoV-2 infection could increase the incidence and severity of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease, in future generations.

Early in the pandemic, researchers observed that people recovering from COVID-19 were not returning to their pre-illness state of health — this is now commonly known as “Long COVID.”

Among the myriad persistent symptoms, many people experience headaches, memory issues, and cognitive deterioration.

Researchers from Northwestern University in Chicago, IL, were the first to report that even non-hospitalized people with COVID-19 demonstrated significant cognitive dysfunction that persisted well beyond 6 weeks from the acute infection.

In the journal Science, Dr. Serena Spudich and Dr. Avindra Nath review our current understanding of the neurologic consequences of COVID-19.

Building on clinical observations, autopsy, and laboratory findings, the authors propose theories of causality about how COVID-19 may result in long-term neurologic symptoms.

Neurologic complications of COVID-19 include:

  • loss of smell (anosmia)
  • stroke
  • delirium — a mental state characterized by an inability to rest, illusions, and incoherent thought and speech patterns
  • encephalopathy — a temporary or permanent state of altered brain function
  • psychiatric symptoms
  • peripheral neuropathy — a condition where nerve damage alters the communication between the central nervous system and the rest of the body

The authors acknowledge that the mechanisms by which COVID-19 can wreak havoc on the human nervous system are not well understood.

Cerebrovascular complications, such as a stroke, can occur early in the infection — even before the respiratory effects of the disease. Central inflammatory conditions and peripheral nerve symptoms occur later, typically 2 weeks after the acute infection.

These disparate timelines suggest that the cause of these neurologic symptoms may differ. Studying the cerebrospinal fluid (CSF) offers clues as to underlying mechanisms for neurologic damage in people with COVID-19.

CSF is a fluid that surrounds the spinal cord and brain.

Scientists have observed increases in certain immune-related compounds in the CSF, including:

  • Interleukin-1 (IL-1) and IL-2 proteins, which are inflammatory cytokines produced by the body.
  • Expression of genes controlled by interferon, an infection-fighting protein present during viral infections.
  • Activated T-cells and natural killer cells, which combat viral antigens.
  • Markers that indicate the presence of monocytes — large white cells that fight infection.
  • Breakdown proteins suggesting nerve damage.

Conversely, researchers have not found evidence that the SARS-CoV-2 virus directly impacts the nervous system. For instance, research has shown that the following factors are reduced or absent in people with a SARS-CoV-2 infection:

  • Cells that cause inflammation are not found clustered around the brain, which normally occurs in cases of viral encephalitis — a swelling of the brain.
  • The CNS does not contain viral RNA.
  • Limited presence of SARS-CoV-2 nucleic acid or viral protein in the brain cells of people who died from COVID-19.

When asked about the lack of virus in the CSF and brain cells, Dr. Santosh Kensari, chair, and professor of translational neurosciences and neurotherapeutics at St. Johns’ Cancer Institute in Santa Monica, CA, commented:

“If the virus isn’t there, it’s not directly [causing] the problem — that would be encephalitis — but the viruses can cause systemic problems, like the inflammation that [can] affect every organ system, including the brain — its an indirect effect.”

Adding and subtracting the positive and negative findings helped the authors of the perspective article to formulate a theory regarding the cause of nervous system consequences of SARS-CoV-2 infection.

They do not rule out that the virus may transiently infect the brain very early in infection. However, the authors ultimately conclude that inflammation and widespread vascular dysfunction may be the vector of neurologic damage in people with COVID-19.

Compared with people with influenza, individuals with COVID-19 exhibit an increased risk of stroke. When scientists studied the blood of people who experienced a stroke, they found elevated blood markers of vascular inflammation, tissue death, and thrombosis, which are clots that obstruct blood flow.

Radiologic testing also provides evidence of injury in people who experienced COVID-19. MRIs confirm microvascular damage and brain atrophy, or shrinkage. Positron emission tomography confirms decreased metabolic activity in the brains of people diagnosed with Long COVID.

This evidence, coupled with the system-wide vascular dysfunction seen in people with severe COVID-19, points to vascular injury as a potential cause of stroke, brain, and nerve injury.

The authors conclude that SARS-CoV-2 is absent and markers of inflammation and vascular dysfunction are increased in the brains of people with COVID-19. So, the effects of COVID-19 are likely the result of an intersection of disease-causing mechanisms:

  • Generalized neuroinflammation supported by the presence of immune cells, cytokines, antibodies, and activated microglia, which are specialized neuron damage-fighting cells.
  • Damage to the cells lining the brain’s blood vessels (endothelium).
  • Elevated levels of blood-clotting proteins.
  • Individual susceptibility, including genetics, preexisting health conditions, and immune strength.

For MNT, Dr. Santosh Kensari addressed why some people might be more susceptible to neuropsychiatric complications from COVID-19 infection.

“I don’t think we know fully, but I suspect it is a variety of factors,” he explained. He believes these probably include the severity of COVID-19 and other cardiovascular risk factors, such as type 2 diabetes.

“My philosophy in medicine has completely changed. For example, inflammation is probably 90{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of aging. Cancer, dementia, all are due to immune function. COVID-19 is making all these things worse because it is driving inflammation.”

– Dr. Santosh Kensari

While laboratory and radiologic evidence support their theories, there is only conjecture on the exact mechanisms at this time.

The authors note that people living with Long COVID may have long lasting immune activation, persistent autoimmune disturbance, or ongoing damage to the endothelium.

Medical experts around the world are worried about the long-term prognosis for people recovering from COVID-19.

From a neurologic standpoint, Dr. Spudich and Dr. Nath are concerned that the neuroinflammation and neuronal injury caused by acute SARS-CoV-2 infection may “accelerate or trigger future development of neurodegenerative diseases, such as Alzheimer’s or Parkinson’s disease.”

And they feel that the neurodevelopmental influences of SARS-CoV-2 infection on children remain unknown.

For MNT, Dr. Santosh Kensari added:

“Chronic inflammation has many causes, including diabetes, obesity, and nutrition. These are a predisposition to autoimmune disorders, and they cause and accelerate the risk of brain-related disorders.”

Given the number of individuals who have experienced COVID-19, the researchers note that the neurologic consequences of COVID-19 represent a global public health problem.

In response to this challenge, the National Institute of Health has established a COVID-19 NeuroDataBank and NeuroBioBank to allow doctors to report and quantify neurologic events from COVID-19.

Drs. Spudich and Nath recommend that rigorous study and interventional trials are needed to dissect why some patients have an acute neurologic illness and others develop chronic disease late in their illness. They propose that understanding the immune dysregulation in individuals with Long COVID holds promise for treatment and long-term management.

For live updates on the latest developments regarding COVID-19, click here.

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Can body fat affect brain aging?

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A current study investigates no matter whether body excess fat may possibly affect cognitive overall performance. BSIP/UIG Via Getty Visuals
  • Being overweight and overweight enhance the chance of numerous health and fitness conditions.
  • A new examine from Canada has identified that surplus overall body pounds might also affect cognitive function, with inflammation maybe actively playing a purpose.
  • Persons with excess fatty tissue gained decreased scores for processing speed in cognitive exams.
  • Bodily training, which raises blood move to the brain, may perhaps aid limit cognitive impairment even in these with a superior physique mass index (BMI).

It is broadly recognised that extra physique weight is involved with lots of wellness disorders. Now, scientists have uncovered an association among adiposity — obtaining way too a lot fatty tissue in the human body — and cognitive impairment.

At the commence of a new review, which appears in JAMA Community Open up, Canadian scientists identified the adiposity of a lot more than 9,000 individuals. They calculated both of those complete entire body body fat and visceral adipose tissue (VAT) — the excess fat that predominantly sits all around organs in the stomach cavity.

Former studies have affiliated VAT, or visceral unwanted fat, with enhanced morbidity and a better mortality danger. Visceral excess fat raises the danger of several conditions, this kind of as:

This most recent review implies that excessive extra fat could have psychological as nicely as actual physical results.

All contributors undertook two cognitive tests — the Electronic Symbol Substitution Test (DSST) and the Montreal Cognitive Assessment (MoCA) — to evaluate a selection of cognitive functions.

The scientists altered the scores for cardiovascular risk factors, academic degree, and MRI-detected vascular brain injuries, which is identified to be linked with cognitive impairment.

The scientists discovered that bigger total body extra fat and better VAT have been both equally noticeably connected with reduced DSST and MoCA scores. The association was larger on the DSST, which assesses processing velocity, than on the MoCA, which is a multidimensional cognitive examination.

Compared with all those in the lowest quartile (25{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}) of adiposity, the efficiency of all those in the optimum quartile was equal to an supplemental 3 yrs of cognitive aging.

These outcomes are not unforeseen, as Dr. Anton Porsteinsson, professor and director of the Alzheimer’s Sickness Care, Analysis and Education Method (Advert-Treatment) at the University of Rochester Healthcare Heart, informed Health care Information Right now:

“It is well-identified that increased adiposity and body fats are linked with increased cardiovascular threat factors and that these are connected with increased danger of cognitive drop. This cross-sectional research observed that extra adiposity was a risk issue for reduced cognitive scores, unbiased of cardiovascular possibility aspects, instructional stage, and MRI-detected vascular brain damage.”

This review reinforces conclusions from a prior analyze of more mature grownups in Dublin, which located an affiliation among adiposity, notably central adiposity, and reduced cognitive operate.

This review can not verify a causative link among adiposity and cognitive impairment, as Dr. Eamon Laird, a senior study fellow at Trinity University Dublin in Ireland, pointed out to MNT:

“It is cross-sectional, and it can be difficult to tease out the associations and detect if visceral adiposity is causative and not just correlated with lowered cognitive scores. But the association is clear.”

The researchers controlled for cardiovascular risk and vascular mind damage, both of those of which investigate has revealed to induce cognitive impairment. So, what else may possibly be dependable for the website link?

The authors counsel that irritation could play a role in cognitive impairment in individuals with over weight or being overweight. Just one current examine involving a lot more than 15,000 people discovered large concentrations of plasma C-reactive protein, an inflammatory marker, in those people with a superior BMI and a superior midsection-hip ratio.

Dr. Porsteinsson agreed with this recommendation, stating, “Systemic swelling and glucose intolerance arise as guide suspects.”

Dr. Laird also supports inflammation getting a role. He said, “Pro-inflammatory cytokines from adipose tissue could also perhaps be contributing to tissue damage by way of swelling.”

There are also other prospective mechanisms. For case in point, “Adiposity can generally go hand in hand with other serious conditions, these types of as hypertension, which could be a individual mechanism,” Dr. Laird explained to MNT.

“Obesity could be linked with lowered blood movement to the mind, which may possibly enhance the threat of vascular microcellular injury, which could direct to [a] reduction in cognitive exam rating,” he additional. In yet another analyze, which Dr. Laird co-authored, scientists uncovered that a 1-centimeter raise in midsection measurement gave the exact same reduction in blood circulation as 1 calendar year of growing older.

This examine confirms former findings that obese and being overweight are involved with cognitive impairment, so what can people do to enable battle this?

Dr. Porsteinsson recommended numerous measures that may well aid: “Weight loss, exercising (the two aerobic and resistance teaching), handle of diabetic issues/glucose intolerance, or speed of processing cognitive schooling are a number of that appear to brain.”

Citing research findings that those with a large BMI or higher waistline-hip ratio who did little physical activity had substantially lower cerebral blood movement, Dr. Laird additional:

“Since physical exercise could likely average weight problems/blood circulation associations, this [increasing physical activity] may well be a price powerful and rather easy way to assistance mitigate the damaging influence of obesity.”

“There are nevertheless several unanswered issues right here, such as why a job of processing velocity (DSST) is additional impacted than a multidimensional cognitive test, so this research begs for more study.”

– Dr. Anton Porsteinsson

In summary, sustaining a reasonable weight could advantage the brain as very well as the system.

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How does heart health affect brain health?

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Updated data from the American Heart Association (AHA) emphasize the crucial link between heart and brain health. Image credit: Hiroshi Watanabe/Getty Images.
  • The 2022 Update of the AHA’s Heart Disease and Stroke Statistics emphasizes the bidirectional relationship between brain and heart health.
  • Globally, the number of dementia cases and deaths has increased alarmingly over the past 3 decades, more than heart disease.
  • Modifying risk factors for cardiovascular disease, such as smoking, diabetes, high blood pressure, obesity, and high cholesterol, may promote healthy aging and prevent cognitive decline.

Current evidence suggests a robust connection between brain health and cardiovascular health. Damage to the heart and blood vessels can increase a person’s risk of stroke and dementia.

A stroke occurs when a clot blocks blood flow or when a blood vessel ruptures in the brain. Strokes cause the death of brain tissue, sometimes resulting in a decline in memory and profound disability.

Additionally, the cumulative effect of multiple small silent strokes — which health experts call ministrokes — can cause vascular dementia. Dementia can have a detrimental impact on memory, cognitive functioning, and personality.

The AHA and the National Institutes of Health (NIH) update vital heart disease and stroke statistics annually. Their joint report highlights data related to important modifiable risk factors affecting cardiovascular health and outcomes associated with the quality of care, procedures, and economic costs for cardiovascular-related conditions.

The AHA Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee recently published “The Heart Disease and Stroke Statistics — 2022 Update: A Report From the American Heart Association” in the AHA’s peer-reviewed journal Circulation.

According to 2020 Global Burden of Disease (GBD) study data, the number of people worldwide with Alzheimer’s disease and related dementias increased at a greater rate than that of people with ischemic heart disease (IHD). From 1990 to 2020, the prevalence of Alzheimer’s disease and related dementias increased about 144{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} globally, compared with 120{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} for IHD.

The study reports more dramatic differences in Alzheimer’s disease and related dementias death rates during the same time frame, with an approximately 185{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} increase in Alzheimer’s disease and related dementias deaths and a 66{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} increase in IHD-related deaths.

A systematic analysis of the 2017 GBD study — the most recent data available — reports that 2.9 million people in the United States had an Alzheimer’s disease or Alzheimer’s disease and related dementias diagnosis.

It is the fourth most prevalent neurological disorder in the U.S., as well as the leading cause of death from neurological disease, surpassing stroke.

There is also a significant economic burden associated with Alzheimer’s disease and related dementias. Between 1996 and 2016, U.S. spending on dementias increased twofold, from about $39 billion to $79 billion.

Dr. Mitchell Elkind, the immediate past president of the AHA, a professor of neurology and epidemiology at Columbia University Vagelos College of Physicians and Surgeons, and attending neurologist at New York-Presbyterian/Columbia University Irving Medical Center in New York, spoke with Medical News Today about the new updates.

“Heart disease and brain disease share many of the same risk factors. Cardiovascular disease risk factors, or the health behaviors and conditions that can lead to heart attacks, include high blood pressure, diabetes, smoking, high cholesterol, and obesity,” he explained.

“For some time, we have known that these same risk factors also lead to strokes, which are injuries to the brain caused by blood vessel — i.e., vascular — disorders. What clinicians, epidemiologists, and other scientists have more recently found is that these same risk factors also contribute to other manifestations of brain disease, such as cognitive decline and dementia, that had not previously been recognized as [a] vascular disorder.”

– Dr. Mitchell Elkind

The 2022 Update highlights the effects of cardiovascular disease risk factors on cognitive dysfunction or dementia development.

In brief, a meta-analysis of 139 studies demonstrated that people with high blood pressure midlife were 55{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} more likely to develop impaired global cognition and about 20{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} more likely to experience impaired executive function, dementia, or Alzheimer’s disease.

Another meta-analysis of four studies found that people with heart failure were 80{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} more likely to develop dementia, while a meta-analysis of 14 studies found that females with diabetes had a 62{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher risk of developing dementia, and males had a 58{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher risk.

In terms of the risk of dementia linked to obesity, a meta-analysis of studies with up to 42 years of follow-up showed that people with midlife obesity had a 33{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} increased risk of developing dementia.

Smoking also remains an important risk factor. A meta-analysis of 37 studies demonstrated that people who smoked at the time had a 30{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} increased risk of dementia, a 40{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher risk of Alzheimer’s disease, and a 38{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} increased risk of vascular dementia.

The risk of cognitive dysfunction or dementia can vary depending on race, ethnicity, sex, education, occupation, and geography.

The 2022 Update highlights an analysis of 2016 Behavioral Risk Factor Surveillance System data that showed that Black adults were about three times more likely and Hispanic adults about four times more likely than white adults to need assistance with daily activities due to memory loss.

Additionally, Alzheimer’s disease and related dementias disproportionately affects females. According to GBD data from 2020, about 20 million males and 35 million females worldwide had a diagnosis of Alzheimer’s disease and related dementias, with a death rate of 1.28 million for females and 0.61 million for males.

Dr. Elkind commented:

“Because nearly half of all adults in the U.S. have elevated blood pressure, and 40{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} are obese, these data provide an inkling of what we can expect to see in the future as the population ages, and the impact of these risk factors begins to be felt. Recent data suggest that globally, dementia cases may triple over the next 3 decades, even as heart disease declines.”

Decreasing risk by modifying lifestyles and behavioral risk factors may help protect people from developing cardiovascular disease, stroke, and dementia. Dr. Elkind stated that a system-wide approach is necessary to achieve long-term behavioral change.

He explained: “Researchers are now testing technologies to see if they can improve our success rates with behavioral risk factors; some of these approaches involve moving the focus of care from the doctor’s office to the home and involving nonphysician providers in management to improve efficiency. For example, can in-home blood pressure monitoring with real-time connection to a doctor or nurse help improve blood pressure?”

Dr. Elkind also wondered: “Can we use nonclinical settings, such as barbershops, to reach Black men and women to detect high blood pressure and make changes in their lifestyles? […] These types of approaches may ultimately lead to bigger benefits than doctors prescribing specific medications or trying to convince individual patients to change their behaviors.”

Dr. Jason Tarpley — a stroke neurologist and director of the Stroke and Neurovascular Center for Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, CA — went on to comment, in an interview with MNT, that “the take-home message is that a lot of this is preventable” through a combination of a healthy diet, exercise, and medications.

He added: “The information age is helping people […] [P]atients know their cholesterol number, they know their LDL, they know their hemoglobin A1C — which is a long-term measurement of their blood sugar — and they know [their] blood pressures. I […] see that behaviors are changing, and I think that people are […] taking more their health into their own hands, and that’s really good.”

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Alzheimer’s and severe COVID-19: Comparing brain damage markers

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Healthcare worker Demetra Ransom comforts a person with COVID-19 at United Memorial Medical Center in Houston, Texas, on December 4, 2020. MARK FELIX/Getty Images
  • A study demonstrated that participants hospitalized with COVID-19 experiencing neurological complications had higher levels of blood proteins or biomarkers associated with neurological damage than people with Alzheimer’s.
  • Increased biomarker levels correlated with COVID-19 severity, mortality risk, and the presence of neurological disorder.
  • Long-term follow-up is necessary to determine if biomarker elevation is associated with an increased risk of developing subsequent neurodegenerative disorders.

COVID-19, the disease that a SARS-CoV-2 infection causes, often brings on mild upper respiratory symptoms. However, some individuals may experience severe illness requiring hospitalization. This can occur due to pneumonia and lung damage causing respiratory failure.

In addition, neurological manifestations commonly occur in people hospitalized with COVID-19. Neurological disorders may include encephalopathy, seizures, stroke, encephalitis, Guillain-Barré syndrome, and acute demyelinating encephalomyelitis.

Researchers at NYU Grossman School of Medicine conducted a study that investigated whether people with COVID-19 experiencing new-onset neurological complications during hospitalization had elevated blood markers indicating neurological damage.

The investigators published study results in the journal Alzheimer’s and Dementia.

Dr. Thomas Wisniewski, M.D., a co-author of the study, professor of neurology, pathology, and psychiatry, and director of both the NYU Alzheimer’s Disease Research Center and the Center for Cognitive Neurology, spoke about the study in an MNT interview.

He explained: “It’s clear that the [SARS-CoV-2] virus has a propensity for inducing vascular damage, targeting in the endothelial cells, and causing disruption of the blood-brain barrier, as well as inducing generalized neuroinflammation. Cytokines like interleukin 6 and interleukin 1 are much elevated in [individuals with COVID-19], and these are cytokines that drive neurodegeneration and Alzheimer’s disease.”

Cytokines are proteins that help the body’s cells to communicate.

Dr. Wisniewski added, “In our study, we became interested in looking at these types of biomarkers, [since these biomarkers] are what we follow in our Alzheimer’s disease research center for looking at the progression of Alzheimer’s-related pathology and other neurodegenerative disorders.”

In an interview with MNT, Jennifer Bramen, Ph.D., a senior research scientist at the Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, CA, who was not involved in the study, described the seven biomarkers the study measured:

  • Total tau and pTau181 are indicators of neuron damage. Their levels increase as AD progresses. In AD, abnormal proteins form tangles, blocking the communication between brain cells, she explained.
  • Ubiquitin C-terminal hydrolase L1 (UCHL1) is an enzyme that breaks down unnecessary proteins in brain cells. Brain injury or neurodegenerative diseases such as AD cause levels of UCHL1 to increase.
  • Increased glial fibrillary acidic protein (GFAP) levels indicate damage to the glial cells. Glial cells help maintain the health of brain cells and the blood-brain barrier, which filters toxic substances.
  • Neurofilament light chain (NfL) measures damage to axons of myelinated neurons. The axon is the part of the neuron that conducts electricity, and myelin is the insulation surrounding the neuron.
  • Amyloid-β (Aβ) 40 and 42 are proteins that build up and cause the formation of amyloid plaques in AD, which disrupt brain cell function and communication.
  • Lastly, a person’s pTau181 to Aβ42 ratio may identify early stages of AD.

Investigators also attempted to determine the association of increased biomarkers with rates of discharge to home and in-hospital death rates.

To assess the level of injury, the researchers compared serum biomarker levels of a control group of participants who had “normal” cognition, mild cognitive impairment (MCI), and AD with the biomarkers of people during hospitalization with COVID-19 and new neurological findings.

Researchers conducted a retrospective analysis of participants enrolled in the Study of Neurologic and Psychiatric Events in Acute COVID-19 (SNaP Acute COVID study), which examined serum samples people gave during their hospitalization for COVID-19.

Dr. Wisniewski explained, “We specifically excluded patients who have a preexisting cognitive disorder, any sort of dementia, or mild cognitive impairment, [to prevent clouding of the results].”

The SNaP Acute COVID study was a prospective study of 4,491 participants conducted in four New York hospitals between March 10 and May 20 of 2020, which evaluated the development of new neurological events during acute COVID-19 hospitalization.

The non-COVID control group comprised blood samples from the NYU Alzheimer’s Disease Research Center clinical core cohort banked before January 1, 2020. This was the date of the first reported COVID-19 cases in New York City. The researchers used validated testing tools — version three of the Uniform Data Set and the Clinical Dementia Rating — to stratify the control participants into three subgroups: normal cognitive functioning, MCI, and AD.

The study measured blood markers using an ultrasensitive testing methodology called single-molecule array technology.

The COVID-19 group consisted of 251 participants with a median age of 71. This group was 63{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} male. There were 161 participants in the control group with a median age of 71. Participants in the control group were 35{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} male.

The most common neurological complications included toxic metabolic encephalopathy (TME) in 63{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of participants and brain injury due to reduced oxygen or blood flow in 46{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}.

The severity of COVID-19 correlated most strongly with total tau, pTau181, and NfL levels.

Higher GFAP and pTau181/Aβ-42 levels were associated with a significantly increased risk of death during hospitalization. Results showed that elevated levels of total tau, NfL, and GFAP corresponded to decreased discharge-to-home rates.

Those participants with COVID-19 who experienced new neurological events during hospitalization had significantly higher total tau, pTau181, NfL, and UCHL1, with the highest levels occurring in those with TME. The participants with COVID-19 had a 179{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} percent higher NfL, 73{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher GFAP, and 13{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher UCHL1 level than the AD group.

Dr. Wisniewski commented:

“In the study, we found very marked elevations of these seven biomarkers, indicating [the] significant presence of neurodegeneration, neuronal death, and gliosis. With marked neurodegeneration, neuroinflammation, and — at least at one time point — elevation of Alzheimer’s disease biomarkers, each […] correlated with the presence of neurological disease and the severity of infection as well as the outcome.”

Dr. Braman stated: “One limitation is that [the study] is only looking at hospitalized patients, so it’s still not clear if these biomarkers might be present in patients with less severe COVID-19 symptoms. Future research would be [needed] to understand how long lasting these effects are and how much they link up with actual cognitive deficits.”

Dr. Wisniewski agreed:

“We have been following these patients for 6 months and one year […] and there was the persistence of cognitive dysfunction [in up to 50{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of these folks]. Hence, it’s important to follow this up. [P]erhaps biomarker findings speak of an increased risk of subsequent neurodegenerative disorders in this population.”

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1 in 100 patients may have brain complications

Artwork showing internal brain anatomy.Share on Pinterest
In people with severe COVID-19, central nervous system complications may be more common than initially estimated. Mental Art + Design/Stocksy
  • A large international study suggests that around 1 in every 100 patients hospitalized with COVID-19 have brain complications.
  • These include stroke, brain hemorrhage, and other potentially fatal conditions.
  • Many of the patients had preexisting illnesses, such as high blood pressure, heart disease, and diabetes.
  • Previous research has shown that some people who recover from COVID-19 have lingering neurological and psychiatric symptoms.

As the COVID-19 pandemic wears on, experts increasingly recognize that SARS-CoV-2, the virus that causes the disease, affects areas beyond the lungs. It can also infect the kidneys, gut, and blood vessels, for example.

In addition, COVID-19 can cause a range of neurological and psychiatric symptoms.

One telltale symptom is a loss of taste or smell, which indicates that SARS-CoV-2 can infect the peripheral nervous system. But the virus can also affect the central nervous system, producing symptoms such as headaches, dizziness, confusion, and seizures.

Now, a large international study led by researchers at Thomas Jefferson University, in Philadelphia, has found that around 1{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of patients hospitalized with COVID-19 develop potentially fatal brain complications.

These include strokes, bleeding, and inflammation called encephalitis.

“Much has been written about the overall pulmonary [lung] problems related to COVID-19, but we do not often talk about the other organs that can be affected,” says Dr. Scott H. Faro, a professor of radiology and neurology at the university, who also led the study.

“Our study shows that central nervous system complications represent a significant cause of morbidity and mortality in this devastating pandemic,” he explains.

The researchers presented their currently unpublished results at the annual meeting of the Radiological Society of North America, in Chicago. The study has yet to be peer reviewed, and only a summary of the results is available.

The retrospective, observational study involved almost 40,000 patients, who were hospitalized with COVID-19 at any of seven university hospitals in the United States or four in Western Europe.

The participants’ average age was 66 years, and there were twice as many men as women.

Many had preexisting conditions, such as heart disease, diabetes, or high blood pressure, which is also called hypertension.

Among those who had undergone a brain MRI or CT scan, 442 patients had brain-related complications attributable to COVID-19.

This suggests that around 1.2{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of the total patient group had a brain complication as a result of the disease.

The most frequent complications were:

  • ischemic stroke: 6.2{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}.
  • hemorrhage, or bleeding: 3.72{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}.
  • encephalitis: 0.47{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}.

More rare complications included inflammation of the brain and spinal cord, which is called acute disseminating encephalomyelitis, and encephalopathy syndrome, which causes symptoms similar to those of a stroke.

“It is important to know an accurate incidence of all the major central nervous system complications,” Dr. Faro says, noting, “There should probably be a low threshold to order brain imaging for patients with COVID-19.”

Overall, brain complications appeared to be about three times as common among patients in Europe, compared with those in the U.S.

The study could not explain the factors behind this disparity. However, doctors detected strokes more often in COVID-19 patients in the U.S. than in Europe.

“The one feature that is likely a contributing factor is: There was an increase in comorbidities (cardiac, diabetes, and chronic [kidney] failure) in the U.S. population [compared with] Europe,” Dr. Faro told Medical News Today.

Currently, the direct role that the viral infection of the central nervous system plays in the neurological complications is unclear.

Overactivation of the immune system, inflammation, dehydration, and low oxygen levels, an issue called hypoxia, are also likely to be important factors.

“The [central nervous system] complications of COVID-19 are multifactorial and [involve] both the direct spread of the virus from the lungs and nasal mucosa, as well as indirect autoimmune factors and physiological changes (hypoxia, inflammation, dehydration),” Dr. Faro told MNT.

“More research is needed to better [understand] this,” he added.

The acute effects of COVID-19 on the central nervous system may result in lingering neurological and cognitive symptoms.

A study published in October found that some people who recover from the infection experience cognitive impairments, such as problems with concentration and memory, often called brain fog, for several months.

There may also be long-term effects on mental health.

A study published in May found that in the 6 months after recovering from COVID-19, 13{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of participants received a first diagnosis of a neurological or psychiatric condition.

The most common diagnoses were anxiety disorders, mood disorders, substance misuse disorders, and insomnia.

Neurological diagnoses were less common, and included strokes, dementia, and brain hemorrhages.

It is unknown whether COVID-19 was directly responsible for these neurological and psychiatric conditions.

The senior author of this study, Paul Harrison, a professor of psychiatry at the University of Oxford, told MNT that he and colleagues are conducting a follow-up study to see whether the effects continue beyond the 6-month period.

“We are looking at longer-term outcomes now and hope to have [our] study completed early next year,” he said.