Dementia: Why we find it difficult to stay awake in the day and sleep at night?

Study Suggests Tau Tangles, Not Amyloid Plaques, Drive Daytime Napping That Precedes Dementia

Researchers and caregivers have noted that excessive daytime napping can develop long before the memory problems associated with Alzheimer’s disease begin to unfold. Prior studies have considered this excessive daytime napping to be compensation for poor nighttime sleep caused by Alzheimer’s-related disruptions in sleep-promoting brain regions, while others have argued that the sleep problems themselves contribute to the progression of the disease. But now UC San Francisco scientists have provided a striking new biological explanation for this phenomenon, showing instead that Alzheimer’s disease directly attacks brain regions responsible for wakefulness during the day.

two people talk in a lab
Lea Grinberg (right), MD, PhD, the senior study author

The new research demonstrates that these brain regions (including the part of the brain impacted by narcolepsy) are among the first casualties of neurodegeneration in Alzheimer’s disease, and therefore that excessive daytime napping – particularly when it occurs in the absence of significant nighttime sleep problems – could serve as an early warning sign of the disease. In addition, by associating this damage with a protein known as tau, the study adds to evidence that tau contributes more directly to the brain degeneration that drives Alzheimer’s symptoms than the more extensively studied amyloid protein.

“Our work shows definitive evidence that the brain areas promoting wakefulness degenerate due to accumulation of tau – not amyloid protein – from the very earliest stages of the disease,” said study senior author Lea T. Grinberg, MD, PhD, an associate professor of neurology and pathology at the UCSF Memory and Aging Center and a member of the Global Brain Health Institute and UCSF Weill Institute for Neurosciences.

Wakefulness Centers Degenerate in Alzheimer’s Brains

In the new study, published August 12, 2019, in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, lead author Jun Oh, a Grinberg lab research associate, and colleagues precisely measured Alzheimer’s pathology, tau protein levels and neuron numbers in three brain regions involved in promoting wakefuless from 13 deceased Alzheimer’s patients and seven healthy control subjects, which were obtained from the UCSF Neurodegenerative Disease Brain Bank.

Compared to healthy brains, Oh and colleagues found that the brains of Alzheimer’s patients had significant tau buildup in all three wakefulness-promoting brain centers they studied – the locus coeruleus (LC), lateral hypothalamic area (LHA), and tuberomammillary nucleus (TMN) – and that these regions had lost as many as 75 percent of their neurons.

portrait on Jun Oh.
Jun Oh, lead author of the study. 

“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” Oh said. “Crucially this means that the brain has no way to compensate because all of these functionally related cell types are being destroyed at the same time.”

Oh and colleagues also studied brain samples from seven patients with progressive supranuclear palsy (PSP) and corticobasal disease (CBD), two distinct forms of neurodegenerative dementia caused by tau accumulation. In contrast to the Alzheimer’s disease brains, wakefulness-promoting neurons appeared to be spared in the PSP and CBD brains, despite comparable levels of tau buildup in these tissue samples.

“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said. “Understanding why this is the case is something we need to follow up in future research.”

Studies Point to Role of Tau Protein in Alzheimer’s Symptoms

The new results are in line with an earlier study by Grinberg’s group which showed that people who died with elevated levels of tau protein in their brainstem – corresponding to the earliest stages of Alzheimer’s disease – had already begun to experience changes in mood, such as anxiety and depression, as well as increased sleep disturbances.

“Our new evidence for tau-linked degeneration of the brain’s wakefulness centers provides a compelling neurobiological explanation for those findings,” Grinberg said. “It suggests we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments.”

These studies add to a growing recognition among some researchers that tau buildup is more closely linked to the actual symptoms of Alzheimer’s than the more widely studied amyloid protein, which has so far failed to yield effective Alzheimer’s therapies.

For instance, another recent study by the Grinberg lab measured tau buildup in the brains of patients who died with different clinical manifestations of Alzheimer’s disease, including variants that involved language impairment or visual problems instead of more typical memory loss. They found that differences in local tau burden in these patients’ brains closely matched their symptoms: patients with language impairments had more tau accumulation in language related brain areas than in memory regions, while patients with visual problems had higher tau levels in visual brain areas.

“This research adds to a growing body of work showing that tau burden is likely a direct driver of cognitive decline,” Grinberg said.

Increased focus on the role of tau in Alzheimer’s suggests that treatments currently in development at UCSF’s Memory and Aging Center and elsewhere that directly tackle tau pathology have the potential to improve sleep and other early symptoms of Alzheimer’s disease, in addition to holding a key to slowing the progress of the disease overall, the authors say.

Authors: See study online for full list of authors.

Funding: This study was supported by The Rainwater Foundation and grants from the National Institutes of Health (R01AG064314, R01AG060477, P50AG023501, P01AG019724, K24AG053435), the Global Brain Health Institute, and the São Paulo Research Foundation (FAPESP).

Disclosures: The authors declare no conflicts of interest.

The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes UCSF Health, which comprises three top-ranked hospitals, as well as affiliations throughout the Bay Area.

Source
August 2019| The Regents of The University of California – Alzheimer’s Disease Destroys Neurons that Keep Us Awake By Nicholas Weiler

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A Better Way to Predict the Progression of Alzheimer’s Disease

News Release
April 2019 | the Society of Nuclear Medicine and Molecular Imaging – New PET Imaging Biomarker Could Better Predict Progression of Alzheimer’s Disease

Reston, VA—Researchers have discovered a way to better predict progression of Alzheimer’s disease. By imaging microglial activation levels with positron emission tomography (PET), researchers were able to better predict progression of the disease than with beta-amyloid PET imaging, according to a study published in the April issue of The Journal of Nuclear Medicine.

According to the Alzheimer’s Association, an estimated 5.3 million Americans are currently living with Alzheimer’s disease. By 2025, that number is expected to increase to more than seven million. The hallmark brain changes for those with Alzheimer’s disease include the accumulation of beta-amyloid plaques. When microglial cells from the central nervous system recognize the presence of beta-amyloid plaques, they produce an inflammatory reaction in the brain.

“The 18-kD translocator protein (TSPO) is highly expressed in activated microglia, which makes it a valuable biomarker to assess inflammation in the brain,” said Matthias Brendel, MD, MHBA, at Ludwig-Maximilians-University of Munich in Germany. “In our study, we utilized TSPO-PET imaging to determine whether microglial activation had any influence on cognitive outcomes in an amyloid mouse model.”

Figure 2Longitudinal TSPO and Aβ PET and performance in behavioral testing. (A) Cortical TSPO PET and Aβ PET signal intensities of PS2APP mice at different ages are expressed as z scores relative to findings in age-matched C57BL/6 mice. Coronal and axial slices are projected on T1-weighted MRI template. (B) Progression of individual TSPO PET z scores and Aβ PET z scores in forebrain of PS2APP mice (n = 10) with age. (C) Differences between PS2APP and C57BL/6 (WT) mice for escape latency (sec) and traveled distance in pixels (pix) as WM readouts. Error bars represent SEM. *P < 0.01. **P < 0.001.

In the study, researchers compiled a series of PET images for 10 transgenic mice with beta-amyloid proteins and seven wild-type mice. TSPO PET imaging of activated microglia was conducted at eight, 9.5, 11.5 and 13 months, and beta-amyloid PET imaging was performed at eight and 13 months. Upon completion of the imaging, researchers then subjected the mice to a water maze in which the mice were to distinguish between a floating platform that would hold their weight and one that would sink. The tasks were performed several times a day during a 1.5-week period. Memory performance in the water maze was assessed by measuring the average travel time from the start point to a platform each day of training and by calculating the traveled distance at the last day of training. After completing the water maze task, immunohistochemistry analyses were performed for microglia, amyloid and synaptic density.

Transgenic mice with the highest TSPO PET signal in the forebrain or other areas associated with spatial learning tended to have better cognitive performance in the water maze, while beta-amyloid signals in the same areas of the brain showed no correlation to cognitive outcomes in the maze. Researchers found that an earlier microglial response to amyloid pathology in transgenic mice also protected synaptic density at follow-up. Specifically, transgenic mice with higher TSPO expression at eight months had much better cognitive outcomes in the water maze and higher synaptic density as confirmed by immunochemistry analyses.

“This study provides the first evidence that the level of microglial activation could be a far better predictor of current and future cognitive performance than beta-amyloid levels,” noted Brendel. “Keeping the limitations of mouse models in mind, it could be crucial to modify an individual’s microglial activation state to ameliorate future cognitive decline. We believe that a balanced microglia activation is crucial for prevention of cognitive impairment.”

The authors of “Early and Longitudinal Microglial Activation but Not Amyloid Accumulation Predicts Cognitive Outcome in PS2APP Mice” include Carola Focke, Maximilian Deussing, Claudio Schmidt, Simon Lindner, Franz-Josef Gildehaus, Leonie Beyer and Barbara von Ungern-Sternberg, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany; Tanja Blume, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, and Center for Neuropathology and Prion Research, Ludwig-Maximilians-University of Munich, Munich, Germany; Benedikt Zott and Helmuth Adelsberger, Institute of Neuroscience, Technical  University of Munich, Munich, Germany; Yuan Shi and Mario M. Dorostkar, Center for Neuropathology and Prion Research, Ludwig-Miximilians-University of Munich, Munich, Germany, and DZNE-German Center for Neurodegenerative Diseases, Munich, Germany; Finn Peters, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany; Gernot Kleinberger, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Biomedical Center, Biochemistry, Ludwig-Maximilians-University of Munich, Munich, Germany; Peter Bartenstein and Matthias Brendel, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, and Munich Cluster for Systems Neurology, University of Munich, Munich, Germany; Laurence Ozmen and Karlheinz Baumann, Roche Pharma Research and Early Development, F. Hoffman-La Roche Ltd., Basel, Switzerland; Christian Haass, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Biomedical Center, Biochemistry, Ludwig-Maximilians-University of Munich, Munich, Germany; Jochen Herms, Center for Neuropathology and Prion Research, Ludwig-Maximilians-University of Munich, Munich, Germany, DZNE-German Center for Neurodegenerative Diseases, Munich, Germany, and Munich Cluster for Systems Neurology, University of Munich, Munich, Germany; Axel Rominger, Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany, Munich Cluster for Systems Neurology, University of Munich, Munich, Germany, and Department of Nuclear Medicine, Inselspital, University Hospital Bern, Bern, Switzerland.

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For more information or to schedule an interview with the researchers, please contact Rebecca Maxey at (703) 652-6772 or 
rmaxey@snmmi.org.  Current and past issues of The Journal of Nuclear Medicine can be found online at http://jnm.snmjournals.org.

About the Society of Nuclear Medicine and Molecular Imaging

The Society of Nuclear Medicine and Molecular Imaging (SNMMI) is an international scientific and medical organization dedicated to advancing nuclear medicine and molecular imaging, vital elements of precision medicine that allow diagnosis and treatment to be tailored to individual patients in order to achieve the best possible outcomes.

SNMMI’s more than 17,000 members set the standard for molecular imaging and nuclear medicine practice by creating guidelines, sharing information through journals and meetings, and leading advocacy on key issues that affect molecular imaging and therapy research and practice. For more information, visit www.snmmi.org.

What good dementia design looks like – A case study on Dementia Training Australia’s work with Scalabrini Village

DTA and Scalabrini Village case study profiled at Alzheimer’s International Conference in Chicago from Dementia Training Australia on Vimeo.

 

A case study on Dementia Training Australia’s work with Scalabrini Village is featured in the program Every Three Seconds, a collaboration between ADI and ITN Productions which highlights the fact that someone in the world is diagnosed with dementia every three seconds.

Source: https://www.dta.com.au/case-studies-dementia-training-australia/

Neglect common in English care homes

News Release
March 21, 2018 | London – Neglect common in English care homes

The largest-ever survey of care home staff in England, led by UCL researchers, has found that neglectful behaviours are widespread.

Elder care

For the study, published today in PLOS ONE, care home staff were asked anonymously about positive and negative behaviours they had done or had witnessed colleagues doing.

Dr Claudia Cooper (UCL Psychiatry), the study’s lead author, said: “We found low rates of verbal and physical abuse; the abusive behaviours reported were largely matters of neglect.

“These behaviours were most common in care homes that also had high rates of staff burnout, which suggests it’s a consequence of staff who are under pressure and unable to provide the level of care they would like to offer.”

From 92 care homes across England, 1,544 care home staff responded to the survey. The staff were asked whether they had, in the past three months, witnessed a range of positive and negative behaviours. Their responses were linked to data from each care home describing a measure of burnout in care home staff.

Some negative behaviours were categorised as ‘abusive’, using a standard definition,* and based on the behaviour reported, rather than the intention of the care home staff. The most common abusive behaviours were: making a resident wait for care (26% of staff reported that happening); avoiding a resident with challenging behaviour (25%); giving residents insufficient time for food (19%); and taking insufficient care when moving residents (11%). Verbal abuse was reported by 5% of respondents, and physical abuse by 1.1%.

At least some abuse was identified in 91 of the 92 care homes.

Positive behaviours were reported to be much more common than abusive behaviours, however some positive but time-consuming behaviours were notably infrequent.  For instance, more than one in three care home staff were rarely aware of a resident being taken outside of the home for their enjoyment, and 15% said activities were almost never planned around a resident’s interests.

“Most care homes, and their staff, strive to provide person-centred care, meaning that care is designed around a person’s needs, which requires getting to know the resident and their desires and values. But due to resources and organisational realities, care can often become more task-focused, despite intentions and aspirations to deliver person-centred care,” said co-author Dr Penny Rapaport (UCL Psychiatry).

“Carers can’t just be told that care should be person-centred – they need to be given the support and training that will enable them to deliver it,” she said.

The study is part of the UCL MARQUE cohort study, which is also looking into cost-effective interventions to improve the quality of care for people with dementia, and will be using this anonymous reporting as a measure of how well training interventions are working.

More than two thirds of care homes residents have dementia. Agitated behaviours such as pacing, shouting or lashing out are more common in dementia, and can make provision of person-centred care very challenging for care staff to deliver, often with minimal training and limited resources.

“With the right training, care home staff may be able to deliver more effective care that doesn’t need to be more expensive or time-consuming. If they understand and know how to respond to behaviour, they may be able to do more without greater resources,” said the study’s senior author, Professor Gill Livingston (UCL Psychiatry).

Dr Doug Brown, Chief Policy and Research Officer at Alzheimer’s Society, commented: “70% of people living in care homes have dementia, and it’s clear from these findings that they’re bearing the brunt of a chronically underfunded social care system.

“It’s upsetting but unsurprising that abusive behaviours were more common in homes with higher staff burnout. We’ve heard through our helpline of people with dementia not being fed, or not getting the drugs they need, because a carer isn’t properly trained, or a care home is too short-staffed.

“By 2021, a million people in the UK will have dementia. The government must act now, with meaningful investment and reform, or we risk the system collapsing completely and people with dementia continuing to suffer needlessly.”

The study was conducted by researchers at UCL and the Camden and Islington NHS Foundation Trust, and funded by the Economic and Social Research Council and the National Institute for Health Research.

Links

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Media contact

Chris Lane

Tel: +44 (0)20 7679 9222

Email: chris.lane [at] ucl.ac.uk

Bilingualism could offset brain changes in Alzheimer’s

A Concordia study sheds light on how language history relates to brain plasticity

News Release
February 6, 2018 | QUEBEC – Bilingualism could offset brain changes in Alzheimer’s

After more than a decade of research, this much we know: it’s good for your brain to know another language.

A new Concordia study goes further, however, focusing specifically on the effects of knowing a second language for patients with Alzheimer’s disease (AD) and mild cognitive impairment (MCI; a risk state for AD).

“Most of the previous research on brain structure was conducted with healthy younger or older adults,” says Natalie Phillips, a professor in the Department of Psychology.

“Our new study contributes to the hypothesis that having two languages exercises specific brain regions and can increase cortical thickness and grey matter density. And it extends these findings by demonstrating that these structural differences can be seen in the brains of multilingual AD and MCI patients.”

Phillips’s study, led by recent Concordia psychology grad Hilary D. Duncan (PhD 17), is soon to be published in Neuropsychologia(Jan, 2018).

New methods: Enter the MRI

Phillips and her team are the first to use high-resolution, whole-brain MRI data and sophisticated analysis techniques to measure cortical thickness and tissue density within specific brain areas.

Namely, they investigated language and cognition control areas in the frontal regions of the brain, and medial temporal lobe structures that are important for memory and are brain areas known to atrophy in MCI and AD patients.

“Previous studies used CT scans, which are a much less sensitive measure,” says Phillips, founding director of Concordia’s Cognition, Aging and Psychophysiology (CAP) Lab.

The study looked at MRIs from participating patients from the Jewish General Hospital Memory Clinic in Montreal.

Their sample included 34 monolingual MCI patients, 34 multilingual MCI patients, 13 monolingual AD patients and 13 multilingual AD patients.

Phillips believes their study is the first to assess the structure of MCI and AD patients’ language and cognition control regions. It is also the first to demonstrate an association between those regions of the brain and memory function in these groups, and the first to control for immigration status in these groups.

“Our results contribute to research that indicates that speaking more than one language is one of a number of lifestyle factors that contributes to cognitive reserve,” Phillips says.

“They support the notion that multilingualism and its associated cognitive and sociocultural benefits are associated with brain plasticity.”

What’s next?

Phillips and her team are already building on their findings.

“Our study seems to suggest that multilingual people are able to compensate for AD-related tissue loss by accessing alternative networks or other brain regions for memory processing. We’re actively investigating that hypothesis now.”

Read the cited study, “Structural brain differences between monolingual and multilingual patients with mild cognitive impairment and Alzheimer disease: Evidence for cognitive reserve.

Source: NEW RESEARCH: Bilingualism could offset brain changes in Alzheimer’s

If you develop Alzheimer’s, will your children get it too?

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Rebecca Sims, Cardiff University

The most common question I get asked is “Will my child get Alzheimer’s disease?” In my experience, this concern is one of the biggest worries for sufferers, and given the devastating effects of the disease, it is not hard to see why it is a difficult thought to contemplate.

For those people with a familial form of Alzheimer’s disease, the answer is quite straightforward. This type of disease is caused by one or more mutation(s) in one of three genes: the amyloid precursor protein (APP), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2). All of these genes are involved in the production of the amyloid protein. This protein accumulates to form sticky buildups known as plaques, which are found between the cells of the Alzheimer brain and are characteristic of disease.

Those of us who are concerned that they may be at risk from familial Alzheimer’s disease can get a definitive answer through one of the many genetic tests available. A single copy of the mutated gene inherited from an affected parent will ultimately cause disease, with symptoms likely to be noticed before the age of 65 and typically between 30 and 60 years of age. Anyone concerned that they may suffer from this form of Alzheimer’s should seek a referral to a genetic counsellor.

Fortunately, families with a familial form of disease represent less than 1% of all families afflicted by this debilitating disease. For the remaining Alzheimer’s disease families, the answer as to the inheritance of disease is much less clear, and disease onset is certainly not inevitable.

Influencing disease

A combination of both genetic and environmental factors, such as age and gender, contribute to non-familial (also known as sporadic) disease risk, but how these risk factors interact and how many risk factors are required to cause disease is still unknown.

The genetics of non-familial Alzheimer’s is complex: we know that nearly thirty genes, common in the general population, influence disease risk, with potentially hundreds more involved. Additionally, two genes of low frequency have consistently been identified, with an imminent publication by the International Genomics of Alzheimer’s Project, showing another two rare genes have a relatively large effect on disease risk.

Perhaps most excitingly for researchers, genetics scientists have shown that four biological processes in Alzheimer’s disease – that were not previously thought to play a casual role in disease onset – are actually involved. The first process is the immune response, in particular the actions of immune cells and how these potentially dysfunction, attacking the brain, which results in brain cell death.

The second is the transport of molecules into the cell, suggesting that there is a mechanism for the movement of damaging proteins into the brain. The third process that has a role in the onset of Alzheimer’s is the synthesis and breakdown of fatty molecules. And the fourth is the processing of proteins that alters protein breakdown, movement, activity and interactions – all of which are essential for normal protein function.

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Lifestyle risk

Age is the greatest risk factor for disease, with the likelihood of developing Alzheimer’s roughly doubling every five years over the age of 65. Women also have more chance of developing the disease than men, potentially due to a reduction in female hormones after menopause.

Medical conditions that increase risk for dementia include cardiovascular factors (type 2 diabetes, high blood pressure, cholesterol levels, and obesity), and depression. While lifestyle factors such as physical inactivity, a diet that increases cholesterol, smoking and excessive alcohol intake, have all been shown to influence disease risk.

Even for those with a high number of genetic, environmental and lifestyle risk factors, Alzheimer’s disease is not inevitable. Likewise, individuals with a low number of risk factors for disease are not precluded from developing Alzheimer’s.

Given this lack of certainty and the lack of effective treatments for Alzheimer’s, most experts don’t recommend genetic testing for non-familial disease. This thinking may well evolve in the future, however, when research identifies new risk genes and improves our understanding of the dysfunctional processes in Alzheimer’s disease.

The Conversation

Answering the burning question, whether you will pass Alzheimer’s disease on to your children, is therefore still a near impossibility. But, as early diagnostic techniques improve, and with the prospect of a number of vaccines and therapeutics currently in clinical trials, risk prediction for Alzheimer’s disease may become mainstream and part of a developing precision medicine culture.

Rebecca Sims, Research Fellow, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University

This article was originally published on The Conversation. Read the original article.

Older Adults Are Still Likely Underestimating Cognitive Impairment in Their Families

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News release

 Study Finds Racial Differences in Reporting and Overall Trend of Underreporting Cognitive Impairment

An increasing number of older adults are reporting cognitive impairment in their families over the past two decades, according to a new study led by researchers at NYU Rory Meyers College of Nursing and East Carolina University’s Brody School of Medicine.

The study, which also finds ethnic and racial differences in reporting cognitive impairment, is published in Preventing Chronic Disease, a journal of the Centers for Disease Control and Prevention.

The aging population in the U.S. is growing rapidly, with the number of people age 65 and over in 2010 (40.2 million) projected to more than double by 2050. With the rapid increase in the aging population, the size of the population with cognitive impairment and dementia will continue to accelerate, highlighting the importance of identifying cognitive changes.

“Cognitive impairment may serve as a precursor to future dementia. Early detection of cognitive impairment can facilitate timely medical treatments, appropriate care planning, and prevention efforts,” said Bei Wu, PhD, Dean’s Professor in Global Health and director of Global Health & Aging Research at NYU Meyers, co-director of NYU Aging Incubator, and the study’s senior author.

The study sought to examine the trends of self-reported cognitive impairment among five major racial/ethnic groups from 1997 to 2015 in the United States. The researchers used data from the National Health Interview Survey, including 155,682 individuals age 60 and above in their sample. The large sample included people of a variety of races and ethnicities, including Asian Americans,  Blacks, Hispanics, Native Americans, non-Hispanic Blacks, and non-Hispanic Whites.

Rather than using a screening test or clinical examination to evaluate cognitive impairment, respondents were asked to report if any family member was “limited in anyway because of difficulty remembering or because of experiencing periods of confusion.”

The researchers found an increasing trend in self-reported cognitive impairment: the overall rate increased from 5.7 percent in 1997 to 6.7 percent in 2015 among older adults in the U.S. This finding may suggest that awareness of cognitive impairment, perhaps from heightened public attention to and interest in Alzheimer’s disease, has improved to some extent.

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When looking at each racial/ethnic group, however, the increasing trend was significant only among White respondents. In Whites, the rate of self-reported cognitive impairment increased from 5.2 percent in 1997 to 6.1 percent in 2015. Asian American, Black, Hispanic, and Native American respondents had higher rates of self-reported cognitive impairment than Whites, but these rates did not significantly increase from 1997 to 2015.

Regardless of the overall increasing trend, the rates of self-reported cognitive impairment were still low, which may suggest underreporting. The researchers note that the rates of self-reported cognitive impairment are much lower than the estimated prevalence of cognitive impairment. For adults 65 years and older, the rate of self-reported cognitive impairment was 6.3 percent in 2000 and 7.5 percent in 2012, while the estimated prevalence of cognitive impairment in the same age group was 21.2 percent in 2000 and 18.8 percent in 2012.

These findings underscore the need to further promote awareness of cognitive impairment, especially in minority populations. Different cultures hold different beliefs and perceptions of disease and aging. For instance, research has found that compared to Whites, minorities are less likely to seek treatment for psychiatric symptoms because of lack of access to care or due to stigma.

“Culturally specific health education is needed in individuals, family members, and healthcare providers to improve awareness and knowledge of signs and early symptoms of Alzheimer’s and other dementia,” said Huabin Luo, PhD, of East Carolina University.

In addition to Wu and Luo, Gary Yu of NYU Meyers coauthored the study.