A Landmark Study Links Herpes 6 and 7 with Alzheimer’s Disease

The findings also showed multiple points of overlap between virus-host interactions and genes associated with Alzheimer's risk

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For the study, published in the journal Nature, the team engineered a hydrogel that can swell those lymphatic vessels.
For the study, published in the journal Nature, the team engineered a hydrogel that can swell those lymphatic vessels. (IANS)

Scientists have found up to two times higher level of human herpes virus among people with Alzheimer’s disease, suggesting the potential role of the viruses in the development of the progressive brain disorder.

Herpes virus causes contagious sores, most often around the mouth or on the genitals.

The study found unusually increased level of human herpesvirus named human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7 ) in the brains of the people with Alzheimer’s than those without the disorder.

“The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence,” said Richard J. Hodes, Director from the US National Institutes of Health.

“Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defense and innate immune function in the pathophysiology of Alzheimer’s,” said Joel Dudley from the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai.

alzheimers
Patient of Alzheimer’s. Pixabay

The findings also showed multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk. Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.

“If it becomes evident that specific viral species directly contribute to an individual’s risk of developing Alzheimer’s or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer’s at individual, as well as population, levels,” Dudley explained.

In the study, published in the journal Neuron, the team initially performed RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer’s to quantify which genes were present in the brain, and whether any were associated with the onset and progression of Alzheimer’s.

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Using different computational approaches, the team uncovered a complex network of unexpected associations, linking specific viruses with different aspects of Alzheimer’s biology.

They examined the influence of each virus on specific genes and proteins in brain cells, and identified associations between specific viruses and amyloid plaques, neurofibrillary tangles, and clinical dementia severity.

Further, they incorporated 800, RNA sequencing samples and observed a persistent increase of HHV-6A and HHV-7 in samples from individuals with Alzheimer’s. (IANS)

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Inflammation in Brain Can Lead to Dementia: Study

Inflammation in the brain linked to several forms of dementia

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Inflammation in the brain may be more widely implicated in dementias than was previously thought. Pixabay

Researchers have revealed that inflammation in the brain may be more widely implicated in dementias than was previously thought. This is a health news.

Inflammation in the brain – known as neuroinflammation – has been recognised and linked to many disorders including depression, psychosis and multiple sclerosis. It has also recently been linked to the risk of Alzheimer’s disease.

For the study, published in the journal Brain, the researchers set out to examine whether neuroinflammation also occurs in other forms of dementia, which would imply that it is common to many neurodegenerative diseases.

The team recruited 31 patients with three different types of frontotemporal dementia (FTD). FTD is a family of different conditions resulting from the build-up of several abnormal ‘junk’ proteins in the brain. “We predicted the link between inflammation in the brain and the build-up of damaging proteins, but even we were surprised by how tightly these two problems mapped on to each other,” said study researcher Thomas Cope from University of Cambridge in the UK.

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For the study, published in the journal Brain, the researchers set out to examine whether neuroinflammation also occurs in other forms of dementia, which would imply that it is common to many neurodegenerative diseases. Pixabay

According to the researchers, patients underwent brain scans to detect inflammation and the junk proteins. Two Positron Emission Tomography (PET) scans each used an injection with a chemical ‘dye’, which lights up special molecules that reveal either the brain’s inflammatory cells or the junk proteins.

In the first scan, the dye lit up the cells causing neuroinflammation. These indicate ongoing damage to the brain cells and their connections. In the second scan, the dye binds to the different types of ‘junk’ proteins found in FTD.

The researchers showed that across the brain, and in all three types of FTD, the more inflammation in each part of the brain, the more harmful build-up of the junk proteins there is. To prove the dyes were picking up the inflammation and harmful proteins, they went on to analyse under the microscope 12 brains donated after death to the Cambridge Brain Bank.

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“There may be a vicious circle where cell damage triggers inflammation, which in turn leads to further cell damage,” sad study researcher Richard Bevan Jones.

The research team stressed that further research is needed to translate this knowledge of inflammation in dementia into testable treatments. (IANS)

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Aerobic Exercise May Help Fight Alzheimer’s Disease: Study

Aerobics may protect against Alzheimer's disease

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Regular aerobic exercise not only improves physical health but also improves cognitive functioning, which might protect against Alzheimer's disease. Pixabay

Researchers have found that regular aerobic exercise not only improves physical health but also improves cognitive functioning, which might protect against Alzheimer’s disease.

“This study is a significant step toward developing an exercise prescription that protects the brain against Alzheimer’s disease, even among people who were previously sedentary,” said lead investigator Ozioma C Okonkwo from University of Wisconsin in the US.

For the study, published in the journal Brain Plasticity, researchers investigated 23 cognitively normal, relatively young older adults with a family history or genetic risk for Alzheimer’s. All patients had a sedentary lifestyle.

They underwent a battery of assessments, including cardiorespiratory fitness testing, measurement of daily physical activity, brain glucose metabolism imaging (a measure of neuronal health), and cognitive function tests.

Alzheimer's aerobics
This research shows that a lifestyle behaviour — regular aerobic exercise — can potentially enhance brain and cognitive functions that are particularly sensitive to Alzheimer’s disease. Pixabay

Half of the participants were randomly assigned to receive information about maintaining an active lifestyle but no further intervention.

The other half participated in a moderate intensity treadmill training program with a personal trainer, three times per week for 26 weeks.

Compared to the participants maintaining their usual level of physical activity, individuals assigned to the active training program improved their cardiorespiratory fitness, spent less time sedentary after the training program ended, and performed better on cognitive tests of executive functioning (but not episodic memory).

Executive function, an aspect of cognition that is known to decline with the progression of Alzheimer’s, comprises the mental processes enabling individuals to plan, focus attention, remember instructions, and juggle multiple tasks successfully.

The participants’ improved cardiorespiratory fitness was associated with increased brain glucose metabolism in the posterior cingulate cortex, an area of the brain linked to Alzheimer’s.

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This research shows that a lifestyle behaviour — regular aerobic exercise — can potentially enhance brain and cognitive functions that are particularly sensitive to the disease.

“The findings are especially relevant to individuals who are at a higher risk due to family history or genetic predisposition,” Okonkwo said. (IANS)

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This Protein in the Human Brain Can Protect Against Alzheimer’s disease

Brain protein that could protect against Alzheimer's disease

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Human Brain
Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease. Pixabay

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results published in the journal Communications Biology suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained study co-author Matthew Macauley, Assistant Professor at University of Alberta in Edmonton, Canada.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” Macauley added.

Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of Alzheimer’s disease.

Brain
CD33 protein in the brain plays a crucial role in modulating the function of microglia. Pixabay

Now, Macauley’s research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia.

“The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said Abhishek Bhattacherjee, first author and postdoctoral fellow in the Macauley lab.

Alzheimer’s disease affects more than 44 million people around the world.

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“These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said Macauley.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse Alzheimer’s disease can be envisioned,” Macauley said. (IANS)