Better memory: Avoid junk food

Study in animals suggests omega-3 may reduce effects

Date:

October 14, 2021

Source:

Ohio State University

Summary:

Four weeks on a diet of highly processed food led to a strong inflammatory response in the brains of aging rats that was accompanied by behavioral signs of memory loss, a new study has found. Researchers also found that supplementing the processed diet with the omega-3 fatty acid DHA prevented memory problems and reduced the inflammatory effects almost entirely in older rats.

    

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Four weeks on a diet of highly processed food led to a strong inflammatory response in the brains of aging rats that was accompanied by behavioral signs of memory loss, a new study has found.

Researchers also found that supplementing the processed diet with the omega-3 fatty acid DHA prevented memory problems and reduced the inflammatory effects almost entirely in older rats.

Neuroinflammation and cognitive problems were not detected in young adult rats that ate the processed diet.

 

Your amazing brain in clear, everyday language

Healing the Brain: Stress, Trauma and Development

“Easy to read. Difficult to put down.”--Micheal J. Colucciello, Jr., NY State pharmaceutical researcher, retired.

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The study diet mimicked ready-to-eat human foods that are often packaged for long shelf lives, such as potato chips and other snacks, frozen entrees like pasta dishes and pizzas, and deli meats containing preservatives.

Highly processed diets are also associated with obesity and type 2 diabetes, suggesting older consumers might want to scale back on convenience foods and add foods rich in DHA, such as salmon, to their diets, researchers say -- especially considering harm to the aged brain in this study was evident in only four weeks.

"The fact we're seeing these effects so quickly is a little bit alarming," said senior study author Ruth Barrientos, an investigator in The Ohio State University Institute for Behavioral Medicine Research and associate professor of psychiatry and behavioral health.

"These findings indicate that consumption of a processed diet can produce significant and abrupt memory deficits -- and in the aging population, rapid memory decline has a greater likelihood of progressing into neurodegenerative diseases such as Alzheimer's disease. By being aware of this, maybe we can limit processed foods in our diets and increase consumption of foods that are rich in the omega-3 fatty acid DHA to either prevent or slow that progression."

The research is published in the journal Brain, Behavior, and Immunity.

Your amazing brain in clear, everyday language

Healing the Brain: Stress, Trauma and Development

“Easy to read. Difficult to put down.”--Micheal J. Colucciello, Jr., NY State pharmaceutical researcher, retired.

​

“David Balog takes a subject fraught with difficulty and makes it simple and accessible to everyone. The book goes a long way in helping one understand how and why and in what ways stress affects how we live and cope. Invaluable.”--Jessica Hudson, former president, National Association of Former Foster Children

ORDER HERE

Barrientos' lab studies how everyday life events -- such as surgery, an infection or, in this case, an unhealthy diet -- might trigger inflammation in the aging brain, with a specific focus on the hippocampus and amygdala regions. This work builds on her previous research suggesting a short-term, high-fat diet can lead to memory loss and brain inflammation in older animals, and that DHA levels are lower in the hippocampus and amygdala of the aged rat brain.

More effective treatment of Alzheimer’s

Alzheimer's is not an inevitable part of aging. 

Treatments, even cures, may be on the way.

 

Date:

September 30, 2021

Source:

Uppsala University

Summary:

Researchers have designed new antibodies that might provide more effective treatment methods for Alzheimer's disease. By designing antibodies that bind even to the smaller aggregates, or clumps, of the amyloid-beta protein, it may be possible to check the progress of the disease.

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Researchers at Uppsala University have designed new antibodies that might provide more effective treatment methods for Alzheimer's disease. By designing antibodies that bind even to the smaller aggregates, or clumps, of the amyloid-beta protein, it may be possible to check the progress of the disease.

 

Your amazing brain in clear, everyday language

Healing the Brain: Stress, Trauma and Development

“Easy to read. Difficult to put down.”--Micheal J. Colucciello, Jr., NY State pharmaceutical researcher, retired.

​

“David Balog takes a subject fraught with difficulty and makes it simple and accessible to everyone. The book goes a long way in helping one understand how and why and in what ways stress affects how we live and cope. Invaluable.”--Jessica Hudson, former president, National Association of Former Foster Children

Developing effective treatment methods for Alzheimer's disease has proved difficult. The most effective, which have just been approved, only provide marginal effects. There are several major reasons why they are not effective, one of which is that the antibodies used do not bind to all the types of toxic clumps that cause Alzheimer's disease.

In Alzheimer's disease, the amyloid-beta protein begins to form clumps. This process is called aggregation, and the clumps created are called aggregates. The research group has previously shown that treatment with the peptide somatostatin causes the body to begin breaking down building blocks of the aggregate. In the new study, the researchers use an antibody that can bind to the toxic aggregates to stop them from harming cells.

The problem with the treatment methods currently tested in patient studies is that the antibodies bind much more strongly to large clumps and hardly at all to small clumps. The small clumps are just as toxic as the large ones and many think that they are actually even more dangerous since they can move more.

The purpose of the current study was to develop an antibody format that can bind to both large and small clumps of amyloid-beta. Antibodies use the avidity effect to bind strongly to their targets. This requires the binding of both arms of the antibody to the same target at the same time.

The distance between the arms of the antibody is crucial for how small an aggregate the antibody can bind to strongly. If the aggregate is smaller than the distance between the arms, they do not bind to the aggregate strongly. If it is larger, they bind to the aggregate very strongly. In the new article, the researchers have developed a new antibody format with shorter distances between the arms so that they bind to smaller aggregates. The new format also has more binding sites to make the binding extra strong.

"Thanks to the avidity effect, the new antibody format is at least 40 times stronger in binding to the clumps. The new type of antibody can also bind to small aggregates with avidity, which we have not previously seen any other antibody do. That is fantastic," says Greta Hultqvist, Senior lecturer and Associate Professor in Protein drug design at Uppsala University who led the study.

The effects of the antibodies were also tested in a cell culture experiment, which showed that the new antibody format could save cells from death caused by amyloid-beta aggregates. Although no pre-clinical experiments were included, the team thinks their results suggest that the new antibody design could be more effective than those trialled so far.

"The focus of the study was targeting the amyloid-beta protein in Alzheimer's disease, but the new antibody design can be general and applicable to other disease-causing clumps. From a long-term perspective, we hope that the new format can open up new avenues for the generation of future treatments, not only in Alzheimer's disease, but also other diseases where proteins start to form aggregates, like Parkinson's disease," says Fadi Rofo, doctoral student and first author of the study.

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Story Source:

Materials provided by Uppsala University. Original written by Elin Bäckström. Note: Content may be edited for style and length.

New hope for Alzheimer's disease, spinal cord injury, more

Date:

August 27, 2020

Source:

DZNE - German Center for Neurodegenerative Diseases

Summary:

Researchers have developed a neurologically acting protein and tested it in laboratory studies. In mice, the experimental compound ameliorated symptoms of certain neurological injuries and diseases, while on the microscopic level it was able to establish and repair connections between neurons. This proof-of-principle study suggests that biologics, which act on neuronal connectivity, could be of clinical use in the long term.

    

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Researchers from the German Center for Neurodegenerative Diseases (DZNE), UK and Japan have developed a neurologically acting protein and tested it in laboratory studies. In mice, the experimental compound ameliorated symptoms of certain neurological injuries and diseases, while on the microscopic level it was able to establish and repair connections between neurons. This proof-of-principle study suggests that biologics, which act on neuronal connectivity, could be of clinical use in the long term. The results are published in the journal Science.

Brain essentials in plain language. Click here.

The human brain's neuronal network undergoes life-long changes in order to be able to assimilate information and store it in a suitable manner. This applies in particular to the generation and recalling of memories. So-called synapses play a central role in the brain's ability to adapt. They are junctions through which nerve signals are passed from one cell to the next. A number of specific molecules -- known as "synaptic organizing proteins" -- make sure that synapses are formed and reconfigured whenever necessary.

An artificial protein

An international team of researchers has now combined various structural elements of such naturally occurring molecules into an artificial protein called CPTX and tested its effect in different disease models. To this end, the compound was administered to mice with neurological deficits that occur in similar fashion in humans. Specifically, the tests focused on Alzheimer's disease, spinal cord injury and cerebellar ataxia -- a disease that is characterized primarily by a failure of muscle coordination. All these conditions are associated with damage to the synapses or their loss. The study was a collaborative effort by experts from several research institutions, including the DZNE's Magdeburg site, MRC Laboratory of Molecular Biology in UK, Keio University School of Medicine in Tokyo, and, also in Japan, Aichi Medical University.

Easing symptoms of disease

"In our lab we studied the effect of CPTX on mice that exhibited certain symptoms of Alzheimer's disease," said Prof. Alexander Dityatev, a senior researcher at the DZNE, who has been investigating synaptic proteins for many years. "We found that application of CPTX improved the mice's memory performance." The researchers also observed normalization of several important neuronal parameters that are compromised in Alzheimer's disease, as well as in the studied animal model. Namely, CPTX increased the ability of synapses to change, which is considered as a cellular process associated with memory formation. Furthermore, CPTX was shown to elevate what is called "excitatory transmission." This is to say that the protein acted specifically on synapses that promoted activity of the contacted cell. And finally, CPTX increased the density of so-called dendritic spines. These are tiny bulges in the cell's membrane that are essential for establishing excitatory synaptic connections.

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Further research by the study partners in the UK and Japan revealed that application of CPTX to mice with motor dysfunction -- caused either by spinal cord injury or pathological conditions similar to cerebellar ataxia -- improved the rodent's mobility. And at the cellular level, the drug was shown to repair and promote excitatory synaptic connections.

A molecular connector

CPTX combines functional domains present in natural synaptic organizing proteins in a unique way. The compound was designed to act as a universal bridge builder for excitatory connections between nerve cells. Where two neurons meet, either in adhesive contact or actually in synaptic connection, CPTX links to specific molecules on the surfaces of both involved cells, and thereby either triggers the formation of new synapses or strengthens already existing ones.

"At present, this drug is experimental and its synthesis, the credit for which goes to our UK partners, is quite demanding. We are far off from application in humans," Dityatev emphasized, who in addition to his research at the DZNE is also a member of the Medical Faculty of the University Magdeburg. "However, our study suggests that CPTX can even do better than some of its natural analogs in building and strengthening nerve connections. Thus, CPTX could be the prototype for a new class of drugs with clinical potential." Application would be in disorders that are associated with impaired neuronal connectivity. "Much of the current therapeutic effort against neurodegeneration focuses on stopping disease progression and offers little prospect of restoring lost cognitive abilities. Our approach could help to change this and possibly lead to treatments that actually regenerate neurological functions. Based on the principles we have used in designing CPTX, we thus intend to develop further compounds. In future studies, we want to refine their properties and explore possible therapeutic applications."

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Breakthrough Test for Alzheimer's

New blood test shows great promise in the diagnosis of Alzheimer's disease

Date:

July 29, 2020

Source:

Lund University

Summary:

A new blood test demonstrated remarkable promise in discriminating between persons with and without Alzheimer's disease and in persons at known genetic risk may be able to detect the disease as early as 20 years before the onset of cognitive impairment, according to a large international study.

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A new blood test demonstrated remarkable promise in discriminating between persons with and without Alzheimer's disease and in persons at known genetic risk may be able to detect the disease as early as 20 years before the onset of cognitive impairment, according to a large international study published today in the Journal of the American Medical Association (JAMA) and simultaneously presented at the Alzheimer's Association International Conference.

For many years, the diagnosis of Alzheimer's has been based on the characterization of amyloid plaques and tau tangles in the brain, typically after a person dies. An inexpensive and widely available blood test for the presence of plaques and tangles would have a profound impact on Alzheimer's research and care. According to the new study, measurements of phospho-tau217 (p-tau217), one of the tau proteins found in tangles, could provide a relatively sensitive and accurate indicator of both plaques and tangles -- corresponding to the diagnosis of Alzheimer's -- in living people.

"The p-tau217 blood test has great promise in the diagnosis, early detection, and study of Alzheimer's," said Oskar Hansson, MD, PhD, Professor of Clinical Memory Research at Lund University, Sweden, who leads the Swedish BioFINDER Study and senior author on the study who spearheaded the international collaborative effort. "While more work is needed to optimize the assay and test it in other people before it becomes available in the clinic, the blood test might become especially useful to improve the recognition, diagnosis, and care of people in the primary care setting."

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Researchers evaluated a new p-tau217 blood test in 1,402 cognitively impaired and unimpaired research participants from well-known studies in Arizona, Sweden, and Colombia. The study, which was coordinated from Lund University in Sweden, included 81 Arizona participants in Banner Sun Health Research Institute's Brain Donation program who had clinical assessments and provided blood samples in their last years of life and then had neuropathological assessments after they died; 699 participants in the Swedish BioFINDER Study who had clinical, brain imaging, cerebrospinal fluid (CSF), and blood-based biomarker assessments; and 522 Colombian autosomal dominant Alzheimer's disease (ADAD)-causing mutation carriers and non-carriers from the world's largest ADAD cohort.

In the Arizona (Banner Sun Health Research Institute) Brain Donation Cohort, the plasma p-tau217 assay discriminated between Arizona Brain donors with and without the subsequent neuropathological diagnosis of "intermediate or high likelihood Alzheimer's" (i.e., characterized by plaques, as well as tangles that have at least spread to temporal lobe memory areas or beyond) with 89% accuracy; it distinguished between those with and without a diagnosis of "high likelihood Alzheimer's" with 98% accuracy; and higher ptau217 measurements were correlated with higher brain tangle counts only in those persons who also had amyloid plaques.

In the Swedish BioFINDER Study, the assay discriminated between persons with the clinical diagnoses of Alzheimer's and other neurodegenerative diseases with 96% accuracy, similar to tau PET scans and CSF biomarkers and better than several other blood tests and MRI measurements; and it distinguished between those with and without an abnormal tau PET scan with 93% accuracy.

In the Colombia Cohort, the assay began to distinguish between mutation carriers and non-carriers 20 years before their estimated age at the onset of mild cognitive impairment.

In each of these analyses, p-tau217 (a major component of Alzheimer's disease-related tau tangles) performed better than p-tau181 (another component of tau tangles and a blood test recently found to have promise in the diagnosis of Alzheimer's) and several other studied blood tests.

In the last two years, researchers have made great progress in the development of amyloid blood tests, providing valuable information about one of the two cardinal features of Alzheimer's. While more work is needed before the test is ready for use in the clinic, a p-tau217 blood test has the potential to provide information about both plaques and tangles, corresponding to the diagnosis of Alzheimer's. It has the potential to advance the disease's research and care in other important ways.

"Blood tests like p-tau217 have the potential to revolutionize Alzheimer's research, treatment and prevention trials, and clinical care," said Eric Reiman, MD, Executive Director of Banner Alzheimer's Institute in Phoenix and a senior author on the study.

"While there's more work to do, I anticipate that their impact in both the research and clinical setting will become readily apparent within the next two years."

Alzheimer's is a debilitating and incurable disease that affects an estimated 5.8 million Americans age 65 and older. Without the discovery of successful prevention therapies, the number of U.S. cases is projected to reach nearly 14 million by 2050.

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Memory Food

Learn about your amazing brain!

Date:

February 18, 2020

Source:

University of Technology Sydney

Summary:

A healthy diet is essential to living well, but should we change what we eat as we age? Researchers have found strong evidence of the link between food groups and memory loss and its comorbidities. Her findings point to a need for age-specific dietary guidelines as the links may vary with age -- people aged 80+ with a low consumption of cereals are at highest risk of memory loss and comorbid heart disease.

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A healthy diet is essential to living well, but as we age, should we change what we eat?

Learn about your amazing brain!

UTS research fellow Dr Luna Xu has studied data from 139,000 older Australians and found strong links between certain food groups, memory loss and comorbid heart disease or diabetes.

Dr. Xu found high consumption of fruit and vegetables was linked to lowered odds of memory loss and its comorbid heart disease. High consumption of protein-rich foods was associated with a better memory.

Dr Xu also found the link between food group and memory status may vary among different older age groups. People aged 80 years and over with a low consumption of cereals are at the highest risk of memory loss and its comorbid heart disease, her research showed.

"Our present study implies that the healthy eating suggestions of cereals consumption in the prevention of memory loss and comorbid heart disease for older people may differ compared to other age groups," said Dr Xu, who holds a Heart Foundation postdoctoral research fellowship.

She said the study pointed to a need for age-specific healthy dietary guidelines.

Memory loss is one of the main early symptoms for people with dementia, which is the second leading cause of death of Australians. People living with dementia have on average between two and eight comorbid conditions, which may accelerate cognitive and functional impairment. The most common comorbidities in dementia include cardiovascular diseases, diabetes and hypertension.

"The dietary intervention in chronic disease prevention and management, by taking into consideration the fact that older populations often simultaneously deal with multiple chronic conditions, is a real challenge," Dr Xu said.

"To achieve the best outcome for our ageing population, strong scientific evidence that supports effective dietary intervention in preventing and managing co-occurring chronic conditions, is essential."

Learn about your amazing brain!

Story Source:

Materials provided by University of Technology Sydney. Note: Content may be edited for style and length.

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Is memory loss inevitable? Book says No.

From Our Memories, Our Selves.

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