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Nov 5, 2019

The 6 Steps You Can Take Now for Brain Health

There are 50 million people worldwide with Alzheimer’s disease, and while much remains mysterious about Alzheimer’s, progress is being made. Many of our researchers are investigating lifestyle activities and interventions to determine which would assist with keeping our brains as healthy as possible for as long as possible.

Dr. Rudy Tanzi of Harvard Medical School, the Chair of the Cure Alzheimer’s Fund Research Leadership Group, says we know more than you might think about how to keep our brains healthy. The good news is that there are proven ways to reduce the inflammation in the brain that is a hallmark of Alzheimer’s disease, and he refers to six steps everyone can take as a SHIELD for their brain.

SLEEP

The impact of sleep on Alzheimer’s disease development has been studied extensively. During sleep, your brain has a natural system for clearing out the debris that builds up and can be destructive, including amyloid beta plaque and tau. When there is too much plaque in the brain, cell function may be compromised and the plaque can bind to nerve cells, harming them over time. Lack of sleep interferes with the brain’s ability to clear the debris. Aim for at least eight hours of sleep each night to ensure your brain has the chance to carry out this cleanup process. “If you are not able to get eight hours of continuous sleep, take naps,” Dr. Tanzi says.

HANDLE STRESS

Studies show that stress affects how the brain functions. Excessive levels of stress can cause and exacerbate disease, in large part through the activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis which elevates cortisol levels. High levels of blood cortisol have a negative impact on memory and can increase levels of inflammation. There is evidence that ongoing, chronic stress may rewire the brain. It is important to find ways to reduce stress. Incorporating relaxation techniques such as meditation into our daily lives can help with overall stress management.

INTERACT

A six-year study published in 2013 with adults older than 65 who had not yet shown cognitive impairment found that those with higher levels of social interaction were less likely to develop dementia. Since this study was finalized, numerous other studies have shown that social interaction preserves cognitive function, as well as a strong connection between loneliness and impaired cognitive function. Numerous studies confirm that older adults with dementia who have a strong social network experience delayed cognitive function. There are many benefits to staying socially active by engaging with friends and family and meeting new people. These include a protective influence on the comprehension and reasoning ability as well as a lower risk of developing symptoms of memory loss. An active social life can open up a new world of opportunity and provide motivation to introduce healthy habits into your life.

EXERCISE

Exercise has been shown to create biochemical changes in the brain related to the health of our nerve cells. In short, exercise facilitates the creation of new nerves and synapses, referred to as neurogenesis, in the hippocampus of the brain. The hippocampus is crucial for memory retrieval and the formation of new memories. Research has found that one of the first areas in the brain affected by Alzheimer’s disease is the hippocampus. Exercise helps prevent atrophy in this area of the brain. The recommendation is to move more: whatever your current level of exercise, just move a little more. Even if you are sedentary, begin by taking a short walk, and increase the length of your walks over time.

LEARN NEW THINGS

In addition to physical exercise, mental exercise is a factor in delaying cognitive decline. Learning new things as we age can keep us mentally sharp and builds our neural networks. For example, reading books, learning a new language or new field of knowledge, practicing memorizing lists or engaging in a new hobby helps keep the brain stimulated. The more challenging and complex, the greater the benefit. “The more synapses you make, the more you can lose before you lose it,” Tanzi says.

DIET

The Mediterranean diet has been shown to benefit your brain the most. That diet emphasizes eating more fruits and vegetables, nuts, olive oil and fish, and reducing consumption of red meat. “The Mediterranean dietis best for your brain,” says Tanzi, adding that your diet has an effect on your microbiome and neuroinflammation.

Dr. Tanzi stresses that making small changes every day can help the health of your brain. “And,” he points out, “these are all things you can do now.”

Aug 13, 2019

Some Brains are Resilient to Alzheimer's Disease

Teresa Gomez-Isla
Teresa Gomez-Isla

Dr. Teresa Gomez-Isla’s lab is on a mission to understand why some unique individuals are able to tolerate severe amounts of the pathological hallmarks of Alzheimer’s disease, including amyloid plaques and neurofibrillary tau tangles, without experiencing dementia. In a research paper supported with a grant from Cure Alzheimer’s Fund, Dr. Gomez-Isla and her colleagues uncovered new insights into what differentiates the brains of these resilient individuals. The research was published in the journal Neurobiology of Disease and makes the case that suppression of the neuroinflammatory response may enhance resilience to dementia.

While the brains of these individuals are riddled with plaques, these rare resilient cases do not exhibit the typical patterns of synapse loss that are normally found in the brains of Alzheimer’s patients. The synapse is the junction between two nerve cells through which neurons communicate either electrically or chemically. These resilient brains provide a rare glimpse into the protective mechanisms that may be at play in individuals who would be expected to have dementia as a result of the heavy burden of plaques and tangles in their brains.

The scientists used markers to determine the levels of microglia and astrocyte activation in the resilient brains compared with the brains of the controls and the brains from individuals who had experienced dementia and Alzheimer’s disease while alive. In an interesting turn of events, the experiment revealed that resilient brains had less activation of two markers: GFAP and CD68. This finding indicated a suppressed neuroinflammatory response in the resilient brains.

Not content to simply show evidence for differences in activation between the two groups, the researchers performed an experiment that profiled 27 different cytokines in the resilient brains and the brains from those with Alzheimer’s disease. Cytokines refer to substances that are secreted by cells in the immune system and regulate other cells. Dr. Gomez-Isla uncovered that not only were the profiles of cytokines in the resilient brains different from the other groups, but the difference was the most pronounced in the entorhinal cortex. The entorhinal cortex is one of the earliest and most severely affected brain regions in Alzheimer’s disease. In the resilient brains that had the highest probability of developing Alzheimer’s disease dementia based on the severity of the plaque accumulation, the cytokine profile showed differences in levels of IL-1b, IL-6, IL13, and IL-4. This data suggests specific cytokine targets that may play a role in enhancing resilience to Alzheimer’s disease.

Teresa Gomez-Isla’s research was highlighted in Harvard Magazine:

https://www.harvardmagazine.com/2019/05/inflammation-disease-diet

Links:

May 15, 2019

A Role for the Immune System in Alzheimer's Disease

Neurodegenerative Diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks. Advances in genetics and animal models across the field, but specifically through the Alzheimer’s Genome Project initiated by Cure Alzheimer’s Fund, are beginning to unearth an unexpected role for the immune system in disease onset and progression. Recent work into the genetics of Alzheimer’s disease has identified a compelling role for immune signaling pathways to play a role in the disease. This lays the ground work for immune-related therapeutic intervention.

Unraveling the genome in order to predict whether someone will get Alzheimer’s disease has been an area of focus for the neurodegenerative disease community. Two back-to-back research papers published in Nature Genetics analyzed the largest-ever genomic data sets to date in order to point to new genetic risk factors for Alzheimer’s disease. Not only that, but the researchers uncovered a role for how these genes contribute to Alzheimer’s disease – in some cases through the immune system. 94,437 individuals who had been diagnosed with late-onset Alzheimer’s disease participated in a genome-wide association study that identified variants in five new genes that put people at risk for Alzheimer’s disease. The data also confirmed 20 other genes that had been previously implicated in Alzheimer’s disease.

Another huge advance from these papers is the identification of the groups of genes that work together to influence risk and disease progression. Many of the genes identified play a role in the formation of beta-amyloid plaques, tau accumulation, and the immune system. The study independently identified ADAM10 and ACE as risk variants for Alzheimer’s disease providing much need replicated support for the findings. By themselves, each of these newly discovered variants contribute only a small amount of increased risk. That being said, this study advances the biological pathways that are involved in the onset and progression of the disease.

This new research paper is ground breaking for those interested in finding a way to predict who will get Alzheimer’s disease later in life. The goal of this research is to understand how the complex biological, environmental, and lifestyle factors interact to contribute to Alzheimer’s.

A “News and Views” piece published in Nature Reviews Neurology by Cure Alzheimer’s Fund researcher Lars Bertram and Chair of the Research Leadership Group of Cure Alzheimer’s Fund, Rudy Tanzi, outlined the major findings of this ground-breaking work. 

Links:

 
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