People with dementia often lose their ability to communicate verbally with loved ones in later stages of the disease. But a Northwestern Medicine study, in collaboration with Institute for Therapy through the Arts (ITA), shows how that gap can be bridged with a new music intervention.
In the intervention — developed at ITA and called “Musical Bridges to Memory” — a live ensemble plays music from a patient’s youth such as songs from the musicals “Oklahoma” or “The Sound of Music.” This creates an emotional connection between a patient and their caregiver by allowing them to interact with the music together via singing, dancing and playing simple instruments, the study authors said.
The program also enhanced patients’ social engagement and reduced neuropsychiatric symptoms such as agitation, anxiety and depression in both patients and caregivers.
More than 6 million people in the U.S. have Alzheimer’s disease.
The study is unusual because it targeted patients with dementia and their caregivers, said lead study author Dr. Borna Bonakdarpour. Most prior studies using music for dementia patients have focused only on the patients.
Which vascular risk factors are associated with the risk of developing dementia may vary with age. A new study shows that among people around age 55, the risk of developing dementia over the next 10 years was increased in those with diabetes and high blood pressure.
For people around 65 years old, the risk was higher in those with heart disease, and for those in their 70s, diabetes and stroke. For 80-year-olds, the risk of developing dementia was increased in those with diabetes and a history of stroke, while taking blood pressure medications decreased the risk.
Working with tiny bacteria, Michigan State University researchers led by Lee Kroos have made a discovery that could have big implications for biology.
The researchers revealed a new way that nature can inhibit or switch off important proteins known as intramembrane proteases — pronounced “pro tea aces” — which the team reported April 26th in the journal eLife.
Although the Spartans made this finding using a model organism, a microbe known as Bacillus subtilis, this type of protein is highly conserved, which is how evolutionary biologists say, “it’s everywhere.”
These types of proteases are found in organisms that span the kingdoms of life, from single-celled bacteria to people. In fact, the first intramembrane protease was discovered in humans in 1997 and perhaps the best-known member of this family, named gamma-secretase, is implicated in Alzheimer’s disease.
Findings open new avenue of research in memory loss
A new Northwestern Medicine study showed cognitive SuperAgers have resistance to the development of fibrous tangles in a brain region related to memory and which are known to be markers of Alzheimer’s disease.
The tangles are made of the tau protein which forms structures that transport nutrients within the nerve cell. These tangles disrupt the cell’s transport system, hampering communication within the neuron and preventing nutrients from performing their particular job within the cell. The end result of tangle formation is cell death.
“The results suggest resistance to age-related tau degeneration in the cortex may be one factor contributing to preserved memory in SuperAgers,” said lead study author Tamar Gefen, an assistant professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine.
The lethargy that many Alzheimer’s patients experience is caused not by a lack of sleep, but rather by the degeneration of a type of neuron that keeps us awake, according to a study that also confirms the tau protein is behind that neurodegeneration.
The study’s findings contradict the common notion that Alzheimer’s patients sleep during the day to make up for a bad night of sleep and point toward potential therapies to help these patients feel more awake.
The data came from study participants who were patients at UC San Francisco’s Memory and Aging Center and volunteered to have their sleep monitored with electroencephalogram (EEG) and donate their brains after they died.
Daytime napping among older people is a normal part of aging – but it may also foreshadow Alzheimer’s disease and other dementias. And once dementia or its usual precursor, mild cognitive impairment, are diagnosed, the frequency and/or duration of napping accelerates rapidly, according to a new study.
The study, led by UC San Francisco, and Harvard Medical School together with Brigham and Women’s Hospital, its teaching affiliate, departs from the theory that daytime napping in older people serves merely to compensate for poor nighttime sleep. Instead, it points to work by other UCSF researchers suggesting that dementia may affect the wake-promoting neurons in key areas of the brain, the researchers state in their paper publishing March 17 in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association.
“We found the association between excessive daytime napping and dementia remained after adjusting for nighttime quantity and quality of sleep,” said co-senior author Yue Leng, MD, PhD, of the UCSF Department of Psychiatry and Behavioral Sciences.
“This suggested that the role of daytime napping is important itself and is independent of nighttime sleep,” said Leng, who partnered with Kun Hu, PhD, of Harvard Medical School, in senior-authoring the paper.
Watch-Like Devices, Annual Evaluations Used to Measure Naps, Cognition
In the study, the researchers tracked data from 1,401 seniors, who had been followed for up to 14 years by the Rush Memory and Aging Project at the Rush Alzheimer’s Disease Center in Chicago. The participants, whose average age was 81 and of whom approximately three-quarters were female, wore a watch-like device that tracked mobility. Each prolonged period of non-activity from 9 a.m. to 7 p.m. was interpreted as a nap.
Good news for those of us who can’t face the day without their morning flat white: a long-term study has revealed drinking higher amounts of coffee may make you less likely to develop Alzheimer’s disease.
As part of the Australian Imaging, Biomarkers and Lifestyle Study of ageing, researchers from Edith Cowan University (ECU) investigated whether coffee intake affected the rate of cognitive decline of more than 200 Australians over a decade.
Lead investigator Dr. Samantha Gardener said results showed an association between coffee and several important markers related to Alzheimer’s disease.
“We found participants with no memory impairments and with higher coffee consumption at the start of the study had lower risk of transitioning to mild cognitive impairment — which often precedes Alzheimer’s disease — or developing Alzheimer’s disease over the course of the study,” she said.
New highly sensitive quantum sensors for the brain may in the future be able to identify brain diseases such as dementia, ALS and Parkinson’s, by spotting a slowing in the speed at which signals travel across the brain. The research findings from a paper led by University of Sussex quantum physicists are published in Scientific Reports journal.
The quantum scanners being developed by the scientists can detect the magnetic fields generated when neurons fire. Measuring moment-to-moment changes in the brain, they track the speed at which signals move across the brain. This time-element is important because it means a patient could be scanned twice several months apart to check whether the activity in their brain is slowing down. Such slowing can be a sign of Alzheimer’s or other diseases of the brain.
In this way, the technology introduces a new method to spot bio-markers of early health problems.
Aikaterini Gialopsou, a doctoral researcher in the School of Mathematical and Physical Sciences at the University of Sussex and Brighton and Sussex Medical School is the lead author on the paper. She says of the discovery:
“We’ve shown for the first time that quantum sensors can produce highly accurate results in terms of both space and time. While other teams have shown the benefits in terms of locating signals in the brain, this is the first time that quantum sensors have proved to be so accurate in terms of the timing of signals too.
The drop in estrogen levels that occurs with menopause brings declines in the volumes of “gray matter,” the cellular matter of the brain, in key brain regions that are also affected in Alzheimer’s disease. But a new study from Weill Cornell Medicine researchers, in collaboration with the University of Arizona, suggests that greater cumulative exposure to estrogen in life, for example from having had more children or from having taken menopause hormone therapy, may counter this brain-shrinking effect.
The findings, reported Nov. 3 in Neurology, come from an analysis of personal histories, MRI scans and cognitive tests on 99 women in their late 40s to late 50s. The researchers confirmed an earlier finding linking menopause to lower gray matter volume (GMV) in brain areas that are vulnerable to Alzheimer’s. But they also linked indicators of higher overall estrogen exposure, such as a longer span of reproductive years (menarche to menopause), more children and the use of menopause hormone therapy and hormonal contraceptives, to higher GMV in some of these brain areas.
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.
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.
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 →