The National Institute on Aging and the Alzheimer’s Association are suggesting changes to the research definition of Alzheimer’s disease. There are new criteria to define what Alzheimer’s disease is and who has it — but only as it relates to clinical trials and research, and not the diagnosis in your doctor’s office, according to Jonathan Graff-Radford, M.D. of the Mayo Clinic.
Previously, Alzheimer’s disease dementia was characterized by symptoms such as memory loss and changes in thinking and cognition. And that’s still the case when your doctor diagnoses Alzheimer’s disease dementia.
Falls are the leading cause of fatal injuries in older adults, causing more than 800,000 hospitalizations and about 30,000 deaths in the U.S. every year. Some risk factors are well-known — advanced age, problems with vision or balance, muscle weakness — but an under-recognized factor is early Alzheimer’s disease. Older people in the earliest stages of Alzheimer’s, before cognitive problems arise, are more likely to suffer a fall than people who are not on track to develop dementia.
Researchers at Washington University School of Medicine in St. Louis have found that, in older people without cognitive problems who experience a fall, the process of neuro-degeneration that leads to Alzheimer’s dementia already may have begun. The findings, available online in the Journal of Alzheimer’s Disease, suggest that older people who have experienced falls should be screened for Alzheimer’s and that new strategies may be needed to reduce the risk of falling for people in the disease’s early stages.
I will repeat, yet again, my extreme interest in the brain aging stemming from the fact that my family has had three cases of dementia or Alzheimer’s Disease. My grandfather, my mother and her sister all had it.
Although it’s normal for brainpower to decline as people age, it’s not inevitable, studies show. Some people remain cognitively sharp into their 80s, 90s, and beyond, defying the common assumption that cognitive decline is a natural part of aging, according to the National Institute on Aging.
These lucky few, called cognitive super agers, perform demonstrably better on memory tests, such as remembering past events or recalling a list of words, compared with other adults their age. NIA-supported researchers are exploring the factors that set these people apart so the knowledge can be used to help others prevent or reverse age-related cognitive decline.
What would you do if you knew how long you had until Alzheimer’s disease set in? Don’t despair. New research from the University of California, Berkeley, suggests one defense against this virulent form of dementia — for which no treatment currently exists — is deep, restorative sleep, and plenty of it.
UC Berkeley neuroscientists Matthew Walker and Joseph Winer have found a way to estimate, with some degree of accuracy, a time frame for when Alzheimer’s is most likely to strike in a person’s lifetime.
“We have found that the sleep you’re having right now is almost like a crystal ball telling you when and how fast Alzheimer’s pathology will develop in your brain,” said Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the paper published, Sept. 3, in the journal Current Biology.
Working with their colleagues at the University of Pennsylvania, researchers at the University of Kentucky have found that they can differentiate between sub-types of dementia inducing brain disease.
“For the first time we created criteria that could differentiate between frontotemporal dementia (FTD) and a common Alzheimer’s ‘mimic’ called LATE disease,” said Dr. Peter Nelson of the Sanders-Brown Center on Aging at the University of Kentucky. He says they validated the criteria rigorously. The study was recently published in BRAIN: A Journal of Neurology. The first author of the paper was John L. Robinson from the University of Pennsylvania and the corresponding author was Nelson.
By now I think everybody reading this blog knows about my family’s connection to Alzheimer’s and dementia. So,it should come as no surprise that I am thrilled to pass on this latest info from the Alzheimer’s Prevention Registry.
A promising new blood test for Alzheimer’s disease is now on the horizon. The newly reported test proved to be just as reliable as more invasive and costly tests at detecting Alzheimer’s and may even be able to detect the disease as long as 20 years prior to symptoms. This is an exciting new development that could make detecting the disease much easier and speed up enrollment in clinical trials.
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 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. Continue reading →
Cognitive decline is a major concern of the aging population. Already, Alzheimer’s disease affects approximately 5.4 million Americans and 30 million people globally. Without effective prevention and treatment, the prospects for the future are bleak. By 2050, it is estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer’s disease is on the rise–recent estimates suggest that Alzheimer’s disease has become the third leading cause of death in the United States behind cardiovascular disease and cancer. Since its first description over 100 years ago, Alzheimer’s disease has been without effective treatment.
While researchers continue to seek out a cure, it is becoming clear that there are effective treatment options. More and more research supports the conclusion that Alzheimer’s disease is not a disease of only Beta Amyloid plaques and Tao tangles but a complex and systemic disease. In this study of patients with varying levels of cognitive decline, it is demonstrated how a precision and personalized approach results in either stabilization or improvement in memory.
Affirmativ Health sought to determine whether a comprehensive and personalized program, designed to mitigate risk factors of Alzheimer’s disease could improve cognitive and metabolic function in individuals experiencing cognitive decline. Findings provided evidence that this approach can improve risk factor scores and stabilize cognitive function.
Do you know that feeling you get in your gut? It turns out your gut may really be trying to tell you something. Our microbiome – the 100 trillion bacteria and organisms living in our gut – appears to have a profound influence on our health and risk of disease. And early scientific studies show there may be a link between the microbiome and the brain that could impact the risk of Alzheimer’s and other brain diseases.
The microbiome is a collection of bacteria, viruses and fungi that live mostly in our intestinal system. They play an important role in digestion and the production of certain vitamins, and they support our immune system. Researchers around the world study the gut microbiome, especially those bacteria unique to individuals, to learn more about their influence on our overall health.
Alzheimer’s disease is a progressive disorder in which the nerve cells (neurons) in a person’s brain and the connections among them degenerate slowly, causing severe memory loss, intellectual deficiencies, and deterioration in motor skills and communication. One of the main causes of Alzheimer’s is the accumulation of a protein called amyloid β (Aβ) in clusters around neurons in the brain, which hampers their activity and triggers their degeneration.
Studies in animal models have found that increasing the aggregation of Aβ in the hippocampus–the brain’s main learning and memory center–causes a decline in the signal transmission potential of the neurons therein. This degeneration affects a specific trait of the neurons, called “synaptic plasticity,” which is the ability of synapses (the site of signal exchange between neurons) to adapt to an increase or decrease in signaling activity over time. Synaptic plasticity is crucial to the development of learning and cognitive functions in the hippocampus. Thus, Aβ and its role in causing cognitive memory and deficits have been the focus of most research aimed at finding treatments for Alzheimer’s.
In the study of people aged over 55, published in Alzheimer’s & Dementia, researchers found ‘repetitive negative thinking’ (RNT) is linked to subsequent cognitive decline as well as the deposition of harmful brain proteins linked to Alzheimer’s.
The researchers say RNT should now be further investigated as a potential risk factor for dementia, and psychological tools, such as mindfulness or meditation, should be studied to see if these could reduce dementia risk.
Lead author Dr Natalie Marchant (UCL Psychiatry) said: “Depression and anxiety in mid-life and old age are already known to be risk factors for dementia. Here, we found that certain thinking patterns implicated in depression and anxiety could be an underlying reason why people with those disorders are more likely to develop dementia.
As the old adage goes, an aspirin a day keeps the doctor away. However, new research shows that an aspirin a day will not keep dementia away.
The ASPREE study, Aspirin in Reducing Events in Elderly, evaluated the use of daily, low-dose aspirin in delaying cognitive decline for healthy older adults. Unfortunately, the study did not find that aspirin had any benefit on reducing memory and thinking problems.
“Aspirin is a commonly used drug known to reduce inflammation.,” explained Joanne Ryan, PhD, who collaborated with her colleagues on ASPREE study. “Since inflammation is a significant factor in Alzheimer’s disease, it formed the basis of the hypothesis that aspirin could be beneficial in helping to reduce the occurrence of cognitive decline.”
The ASPREE study involved more than 19,000 participants, mostly 70 years of age and older, who did not have heart disease or a diagnosis of dementia. Half the participants received 100mg of aspirin daily and half received a placebo. All participants received a series of memory & thinking tests throughout the study.
“At the end of the five year trial, we identified that aspirin had no effect on dementia regardless of ethnicity, age, gender or an individual’s current health.” said Dr. Ryan, head of the Biological Neuropsychiatry and Dementia Unit at Monash University’s School of Public Health and Preventative Medicine in Melbourne, Australia.
The question remains whether aspirin could be beneficial if begun in mid-life, long before Alzheimer’s disease starts to take hold in the brain. Dr. Ryan feels it is possible that the benefits of low-dose aspirin may not be seen for several more years. For that reason, the National Institute on Aging, which funded the ASPREE trial, has sponsored ongoing monitoring of cognitive function and other health measures for the trial’s participants. However, it will be some years before results are known.
“The ASPREE study provides strong evidence that low-dose aspirin will not reduce the risk of Alzheimer’s disease,” said Dr. Ryan. “While the results are disappointing, the findings are very relevant to older people and their physicians and indicate aspirin should not be prescribed solely on the basis of potential cognitive benefits.”
Researchers have found a way to design an antibody that can identify the toxic particles that destroy healthy brain cells – a potential advance in the fight against Alzheimer’s disease.
Their method is able to recognize these toxic particles, known as amyloid-beta oligomers, which are the hallmark of the disease, leading to hope that new diagnostic methods can be developed for Alzheimer’s disease and other forms of dementia.
The team, from the University of Cambridge, University College London and Lund University, designed an antibody which is highly accurate at detecting toxic oligomers and quantifying their numbers. Their results are reported in the Proceedings of the National Academy of Sciences (PNAS).
Older adults who have surgery with general anesthesia may experience a modest acceleration of cognitive decline, even years later. But there’s no evidence of a link to Alzheimer’s disease, according to new research from Mayo Clinic.
The research, published in the British Journal of Anaesthesia, examined brain scans from 585 patients, ages 70 to 91 ― 493 of whom had at least one surgery with general anesthesia. The analysis found cortical thinning in cerebral areas but no significant evidence of deposits of amyloid protein, a hallmark of Alzheimer’s disease. The cortex is the outermost layer of the brain’s nerve cell tissue, and thinning of that tissue is associated with diminished cognitive functions. Continue reading →
Inflammation in the brain may be more widely implicated in dementias than was previously thought, suggests new research from the University of Cambridge. The researchers say it offers hope for potential new treatments for several types of dementia.
Inflammation is usually the body’s response to injury and stress – such as the redness and swelling that accompanies an injury or infection. However, inflammation in the brain – known as neuroinflammation – has been recognized and linked to many disorders including depression, psychosis and multiple sclerosis. It has also recently been linked to the risk of Alzheimer’s disease.
In a study published in the journal Brain, a team of researchers at the University of Cambridge set out to examine whether neuroinflammation also occurs in other forms of dementia, which would imply that it is common to many neurodegenerative diseases.
Herewith another entry in our arsenal against that destroyer of lives – Alzheimer’s Disease, from the Tufts Health & Nutrition Letter.
Alzheimer’s disease accounts for 60 to 80 percent of the loss of memory and other cognitive abilities collectively known as dementia. There is no known food or diet that can prevent or cure Alzheimer’s dementia, but diet may help delay onset and slow progression.
What sets Alzheimer’s apart from other forms of dementia is the excessive buildup of beta-amyloid protein fragments into plaques, as well as defective tau proteins that form tangles in the brain. These changes lead to the death of the nerve cells responsible for everything from memory to movement. There are currently no known dietary factors that can impact the formation of these plaques and tangles, but diet may act in other ways to influence Alzheimer’s and other forms of dementia.