MINNEAPOLIS – A class of drugs used for many conditions, including allergies, colds, high blood pressure and depression, may be associated with an increased risk of developing mild thinking and memory problems, particularly in people who have genetic risk factors for Alzheimer’s disease or markers of this condition, according to a study published in the September 2, 2020, online issue of Neurology®, the medical journal of the American Academy of Neurology. These types of drugs, called anticholinergic drugs, are used for motion sickness, urinary incontinence, overactive bladder, Parkinson’s disease and high blood pressure. There are approximately 100 such drugs in widespread use, with some requiring a prescription and many others that may be purchased over-the-counter. The study found that cognitively normal people taking at least one anticholinergic drug were 47% more likely to develop mild cognitive impairment, which can be a precursor to dementia, over the next decade than people who were not taking such drugs.
Of the 230 people who were taking anticholinergic drugs, 117 people, or 51%, later developed mild cognitive impairment, compared to 192 people, or 42%, of the 458 people who were not taking the drugs. After adjusting for depression, number of medications being taken, and history of cardiac problems, individuals taking at least one anticholinergic drug had a 47% increased risk for developing mild cognitive impairment. Furthermore, those with higher overall exposure to anticholinergic drugs had additional increased risk. Researchers also looked at whether people had had biomarkers for Alzheimer’s disease in their cerebrospinal fluid or had genetic risk factors for Alzheimer’s disease.
Burning more calories linked with greater gray matter volume, reduced Alzheimer’s risk (11 March 2016EurkAlert)
Excerpt– “Whether they jog, swim, garden or dance, physically active older persons have larger gray matter volume in key brain areas responsible for memory and cognition, according to a new study by researchers at the University of Pittsburgh School of Medicine and UCLA.
The findings, published today in the Journal of Alzheimer’s Disease, showed also that people who had Alzheimer’s disease or mild cognitive impairment experienced less gray matter volume reduction over time if their exercise-associated calorie burn was high.
A growing number of studies indicate physical activity can help protect the brain from cognitive decline, said investigator James T. Becker, Ph.D., professor of psychiatry, Pitt School of Medicine. But typically people are more sedentary as they get older, which also is when the risk for developing Alzheimer’s disease and other dementias increases.
Different kinds of physical activity shown to improve brain volume & cut Alzheimer’s risk in half (another 11 March 2016 EurkAlert)
Excerpt- “LOS ANGELES, CA/PITTSBURGH, PA, March 11, 2016: A new study shows that a variety of physical activities from walking to gardening and dancing can improve brain volume and cut the risk of Alzheimer’s disease by 50%.
This research, conducted by investigators at UCLA Medical Center and the University of Pittsburgh, is the first to show that virtually any type of aerobic physical activity can improve brain structure and reduce Alzheimer’s risk. The study, funded by the National Institute of Aging, was published on March 11 in the Journal of Alzheimer’s Disease.”
The AWV was established by 2010’s Affordable Care Act to allow Medicare beneficiaries to receive preventive and assessment services during visits with their primary care providers. And although detection of cognitive impairment is among the required AWV services, no specific tools are mandated and no data are available regarding tools used for this purpose.
The new report outlines a plan for addressing this shortcoming and shows how increased detection leads to earlier and optimal diagnostic evaluation, referral to post-diagnosis support and educational services in the community, and ultimately to improved health-related outcomes and well-being for Medicare beneficiaries with diagnosed dementia and their families.
“The Medicare AWV offers a universal opportunity for primary care providers to start a conversation with older adults and their families about cognitive changes that might be worthy of further investigation,” said Richard Fortinsky, PhD, chair of the workgroup. “Our workgroup’s report provides guidance for providers so they can start this conversation and, as appropriate, employ evidence-based assessment tools to detect cognitive impairment.”
The report is available at www.geron.org/ci. The website also contains a link to a companion webinar held in January, led by workgroup members Katie Maslow, MSW, and Shari M. Ling, MD.
“Increased detection of cognitive impairment is essential for earlier diagnosis of Alzheimer’s disease and related dementia — and also earlier diagnosis leads to more timely linkage of older adults and their families with community-based services and supports,” Maslow said.
In the report, the workgroup outlines a recommended for four-step process achieving its goals.
Step 1 is to kickstart the cognition conversation. To increase detection of cognitive impairment and promote earlier diagnosis of dementia in the Medicare population, the GSA workgroup endorses that primary care providers use the AWV as an annual opportunity to kickstart — that is, to initiate and continue — a conversation with beneficiaries and their families about memory-related signs and symptoms that might develop in older adulthood.
Step 2 is to assess the patient if he or she is symptomatic. The GSA workgroup endorses use of a cognitive impairment detection tool from a menu of tools having the following properties: it can be administered in
five minutes or less; it is widely available free of charge; it is designed to assess age-related cognitive impairment; it assesses at least memory and one other cognitive domain; it is validated in primary care or community-based samples in the U.S.; it is easily administered by medical staff members who are not physicians; and it is relatively free from educational, language, and/or cultural bias. The report provides a list of tools that may be suitable for this purpose.
Step 3 is to evaluate with full diagnostic workup if cognitive impairment is detected. The GSA workgroup recommends that all Medicare beneficiaries who exceed threshold scores for cognitive impairment based on the cognitive assessment tools used in step 2 undergo a full diagnostic evaluation. Numerous published clinical practice guidelines are available to primary care providers and specialists to help them arrive at a differential diagnosis.
Step 4 involves referral to community resources and clinical trials, depending on the diagnosis. The GSA workgroup recommends that all Medicare beneficiaries who are determined to have a diagnosis of Alzheimer’s disease or related dementia be referred to all appropriate and available community services to learn more about the disease process and how to prepare for the future with a dementia diagnosis.
“The GSA workgroup views this suggested four-step process as a framework for communicating with a wide variety of stakeholders about the critical importance of incorporating cognitive impairment detection into everyday clinical practice with older adults,” Fortinsky said. “We look forward to building on this report by helping to plan additional activities intended to disseminate and implement the report’s recommendations in communities throughout the country.”
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The Gerontological Society of America (GSA), the nation’s oldest and largest interdisciplinary organization devoted to research, education, and practice in the field of aging. The principal mission of the Society — and its 5,500+ members — is to advance the study of aging and disseminate information among scientists, decision makers, and the general public. GSA’s structure also includes a policy institute, the National Academy on an Aging Society, and an educational branch, theAssociation for Gerontology in Higher Education.
Courtesy of Dr. Eileen LudersAreas of the brain affected by aging (in red) are fewer and less widespread in people who meditate, bottom row, than in people who don’t meditate.
Since 1970, life expectancy around the world has risen dramatically, with people living more than 10 years longer. That’s the good news.
The bad news is that starting when people are in their mid-to-late-20s, the brain begins to wither — its volume and weight begin to decrease. As this occurs, the brain can begin to lose some of its functional abilities.
So although people might be living longer, the years they gain often come with increased risks for mental illness and neurodegenerative disease. Fortunately, a new study shows meditation could be one way to minimize those risks.
Building on their earlier work that suggested people who meditate have less age-related atrophy in the brain’s white matter, a new study by UCLA researchers found that meditation appeared to help preserve the brain’s gray matter, the tissue that contains neurons
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The researchers cautioned that they cannot draw a direct, causal connection between meditation and preserving gray matter in the brain. Too many other factors may come into play, including lifestyle choices, personality traits, and genetic brain differences.
From the 26 January 2015 University of Indiana press release
INDIANAPOLIS — Whether the adverse cognitive effects of medications can be reversed is of significant importance to an aging population, their caregivers and their families, as well as to an overburdened health care system.
In a commentary in JAMA Internal Medicine, Noll Campbell, Pharm.D., and Malaz Boustani, M.D., MPH, of the Regenstrief Institute and the Indiana University Center for Aging Research, probe the possibility of reversing the adverse cognitive effects of medications frequently prescribed to older adults for chronic conditions including depression, anxiety and incontinence and sold over the counter as allergy and sleep aids.
It is not unusual for older adults to take two, three or more drugs that have a negative impact on their brain function. Over the past decade, Drs. Boustani and Campbell and colleagues have conducted several studies that have found associations between exposure to anticholinergic medications, which block acetylcholine, a nervous system neurotransmitter, and the clinical diagnosis of mild cognitive impairment or dementia. Low levels of acetylcholine have long been implicated in patients with dementia.
In a 2013 study, they reported that drugs with strong anticholinergic effects were associated with a clinical diagnosis of cognitive impairment when taken continuously for as few as 60 days over a one-year period. A similar impact was seen with 90 days of continuous use over a year when taking multiple drugs with weak anticholinergic effect.
In “Adverse Cognitive Effects of Medications: Turning Attention to Reversibility” published in the Jan. 26, 2015, issue of JAMA Internal Medicine, Drs. Campbell and Boustani call for further research to determine whether cognitive impairment caused by the adverse effects of medications can be reversed and to establish the safety risks of discontinuing these medications.
Their commentary accompanies a 10-year observational study by Shelly Gray, Pharm.D., M.S., of the University of Washington and colleagues that reports a higher risk of dementia with increasing dose and duration of exposure to medications with strong anticholinergic activities.
“While the Gray study suggests that adverse cognitive effects of medications were permanent, this may represent the use of dementia as the outcome — a non-reversible condition — rather than a diagnosis of mild cognitive impairment which may be reversible in some older adults. Our previous studies have shown a stronger association of these harmful medications with the diagnosis of mild cognitive impairment than with dementia,” Dr. Campbell said.
“We also differed in populations studied. The Gray study was 91 percent Caucasian, and 66 percent were college educated. Fewer than half had hypertension, and only 8 percent were diabetic. Our study subjects were 60 percent African-American, and nearly all subjects were treated for hypertension, and 3 in 10 had a history of stroke. Higher rates of comorbid disease may explain some of the differences between these studies.”
According to the Alzheimer’s Association, 5 million people with dementia lived in the United States in 2013, accounting for an estimated $214 billion in care costs. With the growth of the aging population, the association estimates that the number of older adults with dementia will be approximately 16 million by 2050, with $1.2 trillion expected in costs of care.
“While the scientific community is actively engaged in the quest, no drugs currently exist to prevent Alzheimer’s disease and other dementing disorders. However, our IU and Regenstrief Institute group has focused on stopping cognitively harmful medications as a safe and cost-effective Alzheimer’s disease prevention,” said Dr. Boustani, who directs the Eskenazi Health Center Healthy Aging Brain Center.
From the 20 January 2015 Penn Medicine press release
JAMA Viewpoint Characterizes Current Model for Treating Mentally Ill as “Ethically Unacceptable and Financially Costly”
PHILADELPHIA — As the United States population has doubled since 1955, the number of inpatient psychiatric beds in the United States has been cut by nearly 95 percent to just 45,000, a wholly inadequate equation when considering that there are currently 10 million U.S. residents with serious mental illness. A new viewpoint in JAMA,written by Dominic Sisti, PhD, Andrea Segal, MS, and Ezekiel Emanuel, MD, PhD, of the department of Medical Ethics and Health Policy in the Perelman School of Medicine at theUniversity of Pennsylvania, looks at the evolution away from inpatient psychiatric beds, evaluates the current system for housing and treating the mentally ill, and then suggests a modern approach to institutionalized mental health care as a solution.
English: Pilgrim Psychiatric Center (Photo credit: Wikipedia)
“For the past 60 years or more, social, political and economic forces coalesced to move severely mentally ill patients out of psychiatric hospitals,” write the authors. They say the civil rights movement propelled deinstitutionalization, reports of hospital abuse offended public consciousness, and new drugs gave patients independence. In addition, economics and federal policies accelerated the transformation because outpatient therapy and drug treatment were less expensive than inpatient care, and the federal legislation like the Community Mental Health Centers Act and Medicaid led to states closing or limiting the size of so-called institutions for mental diseases.
However, the authors write, “deinstitutionalization has really been transinstitutionalization.” Some patients with chronic psychiatric diseases were moved to nursing homes or hospitals. Others became homeless, utilizing hospital emergency departments for both care and housing. But “most disturbingly, U.S. jails and prisons have become the nation’s largest mental health care facilities. Half of all inmates have a mental illness or substance abuse disorder; 15 percent of state inmates are diagnosed with a psychotic disorder.” According to the authors, “this results in a vicious cycle whereby mentally ill patients move between crisis hospitalization, homelessness and incarceration.”
Instead, the authors suggest that a better option for the severely and chronically mentally ill, and the most “financially sensible and morally appropriate way forward includes a return to psychiatric asylums that are safe, modern and humane.” They argue that the term ‘aslyum’ should be understood in its original sense — a place of safety, sanctuary and healing.
“Asylums are a necessary, but not sufficient component of a reformed spectrum of psychiatric services,” write the authors. Reforms need to expand the role of these institutions to address a full range of integrated psychiatric treatment services — from providing care to patients who cannot live alone or are a danger to themselves and others, to providing care to patients with milder forms of mental illness who can thrive with high-quality outpatient care. These fully-integrated, patient-centered facilities do exist in the U.S. today, but more are needed to provide 21st century care to patients with chronic, serious mental illness.
Using a new imaging technique, National Institutes of Health researchers have found that the biological machinery that builds DNA can insert molecules into the DNA strand that are damaged as a result of environmental exposures. These damaged molecules trigger cell death that produces some human diseases, according to the researchers. The work, appearing online Nov. 17 in the journal Nature, provides a possible explanation for how one type of DNA damage may lead to cancer, diabetes, hypertension, cardiovascular and lung disease, and Alzheimer’s disease.
Time-lapse crystallography was used by National Institute of Environmental Health Sciences (NIEHS) researchers to determine that DNA polymerase, the enzyme responsible for assembling the nucleotides or building blocks of DNA, incorporates nucleotides with a specific kind of damage into the DNA strand. Time-lapse crystallography is a technique that takes snapshots of biochemical reactions occurring in cells.
Samuel Wilson, M.D., senior NIEHS researcher on the team, explained that the damage is caused by oxidative stress, or the generation of free oxygen molecules, in response to environmental factors, such as ultraviolet exposure, diet, and chemical compounds in paints, plastics, and other consumer products. He said scientists suspected that the DNA polymerase was inserting nucleotides that were damaged by carrying an additional oxygen atom.
After the DNA polymerase (gray molecule in background) inserts a damaged nucleotide into DNA, the damaged nucleotide is unable to bond with its undamaged partner. As a result, the damaged nucleotide swings freely within the DNA, interfering with the repair function or causing double-strand breaks. These steps may ultimately lead to several human diseases. (Graphic courtesy of Bret Freudenthal)
“When one of these oxidized nucleotides is placed into the DNA strand, it can’t pair with the opposing nucleotide as usual, which leaves a gap in the DNA,” Wilson said. “Until this paper, no one had actually seen how the polymerase did it or understood the downstream implications.”
Last week, I encountered yet another example of why it’s so important to always read the whole study — not just the press release. In this case, it was actually a report, not a study. A press release from Alzheimer’s International with the somewhat misleading headline, “Smoking Increases Risk Of Dementia” arrived in my inbox, citing a new World Health Organization report that put smokers at a 45% higher risk for developing the disease than non-smokers.
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It’s a good reminder that regardless of the reputation of the organization or institution issuing a report, study or press release, read the source information yourself. You never know what you may find.
In this excerpt from Chapter 10, Dr. Rabins focuses on the need for caregivers to have outside help and have time away from the responsibilities of caregiving. He describes how to find good information on available services, how to seek and accept help from friends and neighbors, and how to address problems you may encounter.
You can find this podcast and the rest of the series of podcasts here.
These podcasts are excerpted from a Johns Hopkins University Press audio…
Great component – sharing data! Note below the bolded underlined portion
From the 4 March 2014 press release
The Accelerating Medicines Partnership (AMP) is a bold new venture between the NIH, 10 biopharmaceutical companies and several non-profit organizations to transform the current model for developing new diagnostics and treatments by jointly identifying and validating promising biological targets of disease. The ultimate goal is to increase the number of new diagnostics and therapies for patients and reduce the time and cost of developing them.
AMP will begin with three to five year pilot projects in three disease areas:
For each pilot, scientists from NIH and industry have developed research plans aimed at characterizing effective molecular indicators of disease called biomarkers and distinguishing biological targets most likely to respond to new therapies.
Through this cross-sector partnership, which will be managed through the Foundation for the NIH (FNIH), NIH and industry partners are sharing expertise and resources — $230 million — in an integrated governance structure that enables the best informed contributions to science from all participants. A critical component of the partnership is that industry partners have agreed to make the AMP data and analyses publicly accessible to the broad biomedical community.These pilot projects will set the stage for broadening AMP to other diseases and conditions.
AMP Partners
Government
Industry
Non-Profit Organizations
FDA
NIH
AbbVie
Biogen Idec
Bristol-Myers Squibb
GlaxoSmithKline
Johnson & Johnson
Lilly
Merck
Pfizer
Sanofi
Takeda
Alliance for Lupus Research
Alzheimer’s Association
American Diabetes Association
Lupus Foundation of America
Lupus Research Institute
Foundation for the NIH
Geoffrey Beene Foundation
PhRMA
Rheumatology Research Foundation
USAgainstAlzheimer’s
Budget: 5 years [$230 Million (Rounded) Total Project Funding]
The Accelerating Medicines Partnership (AMP) is a bold new venture between the NIH, 10 biopharmaceutical companies and several non-profit organizations to transform the current model for developing new diagnostics and treatments by jointly identifying and validating promising biological targets of disease. The ultimate goal is to increase the number of new diagnostics and therapies for patients and reduce the time and cost of developing them.
—————————————————
[At the risk of breaking copyright, this came via Twitter]
——————————————-
AMP will begin with three to five year pilot projects in three disease areas:
For each pilot, scientists from NIH and industry have developed research plans aimed at characterizing effective molecular indicators of disease called biomarkers and distinguishing biological targets most likely to respond to new therapies.
Through this cross-sector partnership, which will be managed through the Foundation for the NIH (FNIH), NIH and industry partners are sharing expertise and resources — $230 million — in an integrated governance structure that enables the best informed contributions to science from all participants. A critical component of the partnership is that industry partners have agreed to make the AMP data and analyses publicly accessible to the broad biomedical community. These pilot projects will set the stage for broadening AMP to other diseases and conditions.
AMP Partners
Government
Industry
Non-Profit Organizations
FDANIH
AbbVieBiogen Idec
Bristol-Myers Squibb
GlaxoSmithKline
Johnson & Johnson
Lilly
Merck
Pfizer
Sanofi
Takeda
Alzheimer’s AssociationAmerican Diabetes Association
Lupus Foundation of America
Foundation for the NIH
Geoffrey Beene Foundation
PhRMA
Rheumatology Research Foundation
USAgainstAlzheimer’s
Budget: 5 years [$230 Million (Rounded) Total Project Funding]
The editors of the journal Science have chosen cancer immunotherapy — using the body’s immune system to attack tumors instead of targeting the tumor itself — as the biggest breakthrough of 2013.
“Cancer immunotherapy clinched the #1 spot because it’s causing such a paradigm shift among researchers in how they tackle cancer,” the journal’s editorial team wrote in a statement.
The technique involves training immune cells to recognize the characteristics of cancer cells, and then fight back. There’s still a lot of work ahead since the treatment has only worked for a few patients and some types of cancers so far, but the results from clinical trials offer hope for a new weapon against cancer.
Nine other groundbreaking achievements that were chosen from this year are detailed below.
Scientists discover the first real reason we need sleep
By studying a newfound pathway in mice, scientists identified the first major mechanical reason we need to sleep: to clean the brain. When the brain is sleeping, channels between cells grow. This allows cerebrospinal fluid into the depths of the brain tissues to flush out toxic proteins that build up during the day, including the kind that are responsible for neurodegenerative diseases like Alzheimer’s.
A team led by a longtime Oregon Health & Science University researcher has demonstrated in mice what could be a revolutionary new technique to cure a wide range of human diseases — from cystic fibrosis to cataracts to Alzheimer’s disease — that are caused by “misfolded” protein molecules
Misfolded protein molecules, caused by gene mutation, are capable of maintaining their function but are misrouted within the cell and can’t work normally, thus causing disease. The OHSU team discovered a way to use small molecules that enter cells, fix the misfolded proteins and allow the proteins to move to the correct place and function normally again.
The researchers were led by P. Michael Conn, Ph.D., who was a senior scientist in reproductive sciences and neuroscience at OHSU’s Oregon National Primate Research Center and professor of physiology and pharmacology, cell biology and development and obstetrics and gynecology at OHSU for the past 19 years. This month, Conn joined Texas Tech University Health Sciences Center as senior vice president for research and associate provost.
The team’s work will be published this week in the early online edition of the Proceedings of the National Academy of Sciences. The work was the culmination of 13 years of work on the process by Conn and Jo Ann Janovick, former senior research associate at the ONPRC who is now also at TTUHSC. Richard R. Behringer, Ph.D., from the University of Texas MD Anderson Cancer Center, M. David Stewart, Ph.D., from the University of Houston, and Douglas Stocco, Ph.D., and Pulak Manna, Ph.D., from the department of biochemistry/microbiology at TTUHSC, also contributed to the work.
Conn and his team perfected the process in mice, curing them of a form of disease that causes males to be unable to father offspring. The identical disease occurs in humans and Conn believes the same concept can work to cure human disease as well.
“The opportunity here is going to be enormous,” said Conn, “because so many human diseases are caused by misfolded proteins. The ability of these drugs — called ‘pharmacoperones’ — to rescue misfolded proteins and return them to normalcy could someday be an underlying cure to a number of diseases. Drugs that act by regulating the trafficking of molecules within cells are a whole new way of thinking about treating disease.”
…
A wide range of diseases are caused by an accumulation of misfolded proteins. Among the diseases are neurodegenerative diseases like Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. Other diseases include certain types of diabetes, inherited cataracts and cystic fibrosis.
Conn said the next steps will be clinical trials to see whether the same technique can work in humans.
CBS News online actually asked whether a scoop of peanut butter and a ruler could become the “elusive”…”single..definitive test” that could determine whether a person has Alzheimer’s disease.
Reading CBS News’s headline, “Cheap Alzheimer’s Test Made From Peanut Butter and Ruler, Researchers Report,” reminded me of the old adage “Fast, good, or cheap: Pick two.”
A couple things made me wonder just how much of an advance this was:
The study was small, fewer than 100 people all together, divided into four groups ranging from probable Alzheimer’s to healthy controls.
The journal — which is not exactly a core clinical title — is ranked in the bottom third of neuroscience journals by Thomson Scientific’s impact factor, 162 out of 252. Wouldn’t the researchers have tried for a more prestigious, and clinical, journal first?
So we asked a range of Alzheimer’s researchers what they thought. Here’s a sampling:
Richard Caselli, MD, of the Mayo Clinic, Scottsdale: “I don’t think anyone will feel comfortable diagnosing AD on the basis of a smell test.”
Samuel Gandy, of Mount Sinai School of Medicine: “Smell tests for dementia screening have been proposed for years, but the lack of specificity has repeatedly undone the early claims. Ditto for eye tests. This might be the exception, but I would urge caution pending independent replication on larger numbers and diversities of subjects.”
George Bartzokis, MD, UCLA: “Do not dismiss the study. What is new here is simply what they used to test it out — peanut butter. The principal problem with smell tests is that they are nonspecific and therefore only one small piece of the diagnostic puzzle. Not only can you have some congestion in your nasal cavities that can reduce your smell on a temporary basis but a past head trauma, severe past sinus infections, etc. can do so on a permanent basis. Individuals may not even remember these past events or be aware of current sinus problems that could interfere with their ability to smell.”
I wouldn’t suggest that anyone dismiss the study. But I would suggest that they dismiss much of the news coverage of the study. Sampling of other headlines:
“Now, for example, we no longer have to rely on autopsies to confirm the existence of Alzheimer’s plaques. In a major advance last year, the Food and Drug Administration approved a method that uses a radioactive dye, known commercially as Amyvid, to light up amyloid plaques in a PET scan.”
Some journalists love such stories. PET produces bright, colorful images. It’s “good news” for Alzheimer’s, as the Washington Post headline stated, right?
“At present, the medical literature provides extremely limited data with which to evaluate the clinical utility of Aβ (amyloid-β) PET. There are reasonable data showing that, when read by well-trained interpreters, Aβ PET is highly accurate in determining whether there is amyloid in the brain. However, the clinical utility of a positive scan result remains uncertain. If tested, approximately one-third of cognitively normal older adults would have a “positive” test result for brain amyloid. Thus a positive Aβ PET result is not diagnostic of AD, nor can the test be used to accurately predict the risk or the timing of progression of mild cognitive impairment.
The clinical utility of a negative Aβ PET result seems greater than the clinical utility of a positive result because the high sensitivity of a negative test result allows AD to be effectively ruled out as the cause of a patient’s cognitive impairment. It remains uncertain, however, if negative test results lead to important changes in subsequent clinical management or whether any such changes would produce net health benefits for patients and families. Even if negative test results would produce net benefits, rigorous evaluations of Aβ PET must consider the overall balance of benefits and harms of both positive and negative test results in broadly representative patient populations. The current literature on Aβ PET imaging for AD is insufficient to provide this level of evidence. Given the limited effectiveness of the targeted treatments for AD that are currently available, demonstrating that Aβ PET leads to changes in clinical impressions and intended management is insufficient. More persuasive evidence that Aβ PET improves patient outcomes is needed.”
“Clearly, more data are needed about the role of Aβ PET in the prevention, diagnosis, and treatment of patients with AD. At present, the evidence tells us that the role of the scans is uncertain in many situations. The test could aid diagnosis and management in some circumstances, but it could also be harmful in other circumstances; for example, if a positive scan result leads to labeling a person as having a dread and incurable disease and that potential diagnosis turns out to be wrong.”
Why wouldn’t this paper and this editorial receive the same kind of attention as the “good news” stories highlighted above? Don’t journalists see the huge public policy issues at stake here? It’s difficult to understand. If you’re that committed to reporting on imaging tests for Alzheimer’s that you are scouring the journal Neuron, for example, wouldn’t you consider these articles newsworthy as well? If not, why not?
A team of Columbia University Medical Center (CUMC) researchers, led by Nobel laureate Eric R. Kandel, MD, has found that deficiency of a protein called RbAp48 in the hippocampus is a significant contributor to age-related memory loss and that this form of memory loss is reversible. The study, conducted in postmortem human brain cells and in mice, also offers the strongest causal evidence that age-related memory loss and Alzheimer’s disease are distinct conditions.
…….
“The fact that we were able to reverse age-related memory loss in mice is very encouraging,” said Dr. Kandel. “Of course, it’s possible that other changes in the DG contribute to this form of memory loss. But at the very least, it shows that this protein is a major factor, and it speaks to the fact that age-related memory loss is due to a functional change in neurons of some sort. Unlike with Alzheimer’s, there is no significant loss of neurons.”
Finally, the study data suggest that RbAp48 protein mediates its effects, at least in part, through the PKA-CREB1-CBP pathway, which the team had found in earlier studies to be important for age-related memory loss in the mouse. According to the researchers, RbAp48 and the PKA-CREB1-CBP pathway are valid targets for therapeutic intervention. Agents that enhance this pathway have already been shown to improve age-related hippocampal dysfunction in rodents.
“Whether these compounds will work in humans is not known,” said Dr. Small. “But the broader point is that to develop effective interventions, you first have to find the right target. Now we have a good target, and with the mouse we’ve developed, we have a way to screen therapies that might be effective, be they pharmaceuticals, nutraceuticals, or physical and cognitive exercises.”
“There’s been a lot of handwringing over the failures of drug trials based on findings from mouse models of Alzheimer’s,” Dr. Small said. “But this is different. Alzheimer’s does not occur naturally in the mouse. Here, we’ve caused age-related memory loss in the mouse, and we’ve shown it to be relevant to human aging.”
Music as a healing mechanism has been accepted for over 50 years. Music is a source of primal memory similar to that of smell. It has been used in brain injury patient management, as well as to promote wellness, manage stress alleviate pain, promote physical rehabilitation, and enhance memory in Alzheimer’s Disease patients.I have appreciated the power of music my whole life and as a physician and musician, realized its healing potential early on in my medical career. I burned CDs of the music chosen by my patients to be played during their surgery (usually performed with light sedation) and gave it to them as a surprise at their office follow-up visit.
I will lightly touch on some reasons why music would be a great digital health technology.
1. There are scientific studies to provide evidence of efficacy. There are very few digital health technologies that are mobile technologies which have been proven to be efficacious. Since music has been digital for decades, it is a natural for adoption as a mobile health tech tool. Here’s a nice bibliography on the uses of music therapy. Areas such as mental health, special education and Autism, and pain management have been subjects of studies.
English: PET scan of a human brain with Alzheimer’s disease (Photo credit: Wikipedia)
Along the lines of what I’ve been thinking for a few years..symptoms and tests can “point”, but not always
indicate with 100% accuracy. Signs of disease are not always “proof” of disease.
It is possible to both have and not have Alzheimer’s disease. Contradictory as this statement is, a study reported from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) supports it.
In a paper published in the October issue of the Annals of Neurology investigators reported the results of biomarker studies of 53 patients with dementia caused by Alzheimer’s disease. They found a notable proportion of these patients lacked one of the signature pathologies: brain amyloid. This result has notable scientific and policy implications…..
UCLA researchers have for the first time measured the activity of a brain region known to be involved in learning, memory and Alzheimer’s disease during sleep. They discovered that this part of the brain behaves as if it’s remembering something, even under anesthesia, a finding that counters conventional theories about memory consolidation during sleep.
Mehta and his team looked at three connected brain regions in mice — the new brain or the neocortex, the old brain or the hippocampus, and the entorhinal cortex, an intermediate brain that connects the new and the old brains. While previous studies have suggested that the dialogue between the old and the new brain during sleep was critical for memory formation, researchers had not investigated the contribution of the entorhinal cortex to this conversation, which turned out to be a game changer, Mehta said. His team found that the entorhinal cortex showed what is called persistent activity, which is thought to mediate working memory during waking life, for example when people pay close attention to remember things temporarily, such as recalling a phone number or following directions.
“The big surprise here is that this kind of persistent activity is happening during sleep, pretty much all the time.” Mehta said. “These results are entirely novel and surprising. In fact, this working memory-like persistent activity occurred in the entorhinal cortex even under anesthesia.”
The study appears Oct. 7, 2012 in the early online edition of the journal Nature Neuroscience.
The findings are important, Mehta said, because humans spend one-third of their lives sleeping and a lack of sleep results in adverse effects on health, including learning and memory problems.
It had been shown previously that the neocortex and the hippocampus “talk” to each other during sleep, and it is believed that this conversation plays a critical role in establishing memories, or memory consolidation. However, no one was able to interpret the conversation…..
For older adults, loneliness is a major risk factor for health problems — such as cardiovascular disease and Alzheimer’s — and death. Attempts to diminish loneliness with social networking programs like creating community centers to encourage new relationships have not been effective.
However, a new study led by Carnegie Mellon University’s J. David Creswell offers the first evidence that mindfulness meditation reduces loneliness in older adults. Published in Brain, Behavior & Immunity, the researchers also found that mindfulness meditation — a 2,500-year-old practice dating back to Buddha that focuses on creating an attentive awareness of the present moment — lowered inflammation levels, which is thought to promote the development and progression of many diseases. These findings provide valuable insights into how mindfulness meditation training can be used as a novel approach for reducing loneliness and the risk of disease in older adults.
“We always tell people to quit smoking for health reasons, but rarely do we think about loneliness in the same way,” said Creswell, assistant professor of psychology within CMU’s Dietrich College of Humanities and Social Sciences. “We know that loneliness is a major risk factor for health problems and mortality in older adults. This research suggests that mindfulness meditation training is a promising intervention for improving the health of older adults.”…
Six months ago, researchers at UCLA published a study that showed using a specific type of yoga to engage in a brief, simple daily meditation reduced the stress levels of people who care for those stricken by Alzheimer’s and dementia. Now they know why.
As previously reported, practicing a certain form of chanting yogic meditation for just 12 minutes daily for eight weeks led to a reduction in the biological mechanisms responsible for an increase in the immune system’s inflammation response. Inflammation, if constantly activated, can contribute to a multitude of chronic health problems.
This article resonates with me.
When my father was dying, it was a struggle not to help too much..and to make sure he made the decisions he was capable of, and physically moved on his own as much as possible.
Last week, as part of my volunteering at a senior residential center, I took a resident shopping. Although she had recently returned from the hospital, I did insist she go into the store with me (I was thinking exercise, she doesn’t move around much) …on the pretense that although she had a list, that would be the only way she would be assured she’d get what she needed.
She did manage! and thankfully wasn’t in pain (at least she didn’t complain).
As a volunteer at our local Area Office on Aging, it is challenging to offer options, but allow the clients to make their own decisions. Active listening is hard at times, but it does pay off in the end.
Family members or professional caregivers who do everything for older adults withAlzheimer’s disease may just be wanting to help, but one University of Alberta researcher says that creating excess dependency may rob the patients of their independence and self-worth.
U of A psychologist Tiana Rust, who recently completed her doctoral program, says her research indicated that caregivers adopted a “dependency support script,” assuming control of tasks they believed patients seemed no longer capable of doing for themselves. She says this model shows that the caregivers’ beliefs, rather than the person’s real abilities, drove their interactions with the patients. Her research also showed that the caregivers’ actions were also seemingly incongruous with their values of wanting to treat patients with respect and promote their independence.
With an aging Canadian population, the number of people suffering from the disease is expected to increase over the next 20 years, she says. Thus, changing behaviour becomes critical – and she’s hoping her U-of-A based research will help spark that change.
“When we create this excess dependency that doesn’t need to be there, this is a problem,” said Rust. “1.1 million Canadians are projected to have dementia by 2038. So, if we’re able to maintain and promote independence to the degree permissible by the disease, that’s important.”
What do heart disease, diabetes, Alzheimer’s, stroke and cancer have in common? Scientists have linked each of these to a condition known as chronic inflammation, and they are studying how high-fat foods and excess body weight may increase the risk for fatal disorders.
While much focus has been on fighting inflammation with drugs, researchers are getting a better understanding of the links connecting diet, inflammation and illness and discovering ways that foods can help keep inflammation in check. Laura Landro has details on Lunch Break.
Inflammation is the body’s natural response to injury and outside irritants. But when the irritants don’t let up, because of a diet of high-fat foods, too much body fat and smoking, for example, the immune system can spiral out of control and increase the risk for disease. Experts say when inflammation becomes chronic it can damage heart valves and brain cells, trigger strokes, and promote resistance to insulin, which leads to diabetes. It also is associated with the development of cancer.
Much of the research on chronic inflammation has focused on fighting it with drugs, such as cholesterol-lowering statins for heart disease. A growing body of research is revealing how abdominal fat and an unhealthy diet can lead to inflammation. Some scientists are investigating how certain components in foods might help. Dietary fiber from whole grains, for instance, may play a protective role against inflammation, a recent study found. And dairy foods may help ease inflammation in patients with a combination of risk factors…
…A substance known as C-reactive protein, measured with a simple blood test, is an indicator of inflammation in the body. A report published in Archives of Internal Medicine in 2007, which analyzed results of 33 separate studies, found that losing weight can lower C-reactive protein levels. For each one kilogram, or 2.2 pounds, of weight loss, whether by dieting, exercise or surgery, the mean reduction in C-reactive protein among participants was 0.13 milligram per liter…
..At a meeting in Quebec City last week on abdominal obesity and its health risks, experts in cardiology, endocrinology, nutrition and related specialties presented a wide range of new research linking obesity to inflammation-related diseases…
Every day we make thousands of tiny predictions when the bus will arrive, who is knocking on the door, whether the dropped glass will break. Now, in one of the first studies of its kind, researchers at Washington University in St. Louis are beginning to unravel the process by which the brain makes these everyday prognostications. While this might sound like a boon to day traders, coaches and gypsy fortune tellers, people with early stages of neurological diseases such as schizophrenia, Alzheimer’s and Parkinson’s diseases could someday benefit from this research…
This blog presents a sampling of health and medical news and resources for all. Selected articles and resources will hopefully be of general interest but will also encourage further reading through posted references and other links. Currently I am focusing on public health, basic and applied research and very broadly on disease and healthy lifestyle topics.
Several times a month I will post items on international and global health issues. My Peace Corps Liberia experience (1980-81) has formed me as a global citizen in many ways and has challenged me to think of health and other topics in a more holistic manner.
Do you have an informational question in the health/medical area? Email me at jmflahiff@yahoo.com I will reply within 48 hours.
My professional work experience and education includes over 15 years experience as a medical librarian and a Master’s in Library Science. In my most recent position I enjoyed contributing to our library’s blog, performing in depth literature searches, and collaborating with faculty, staff, students, and the general public.
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Courtesy of Dr. Eileen LudersAreas of the brain affected by aging (in red) are fewer and less widespread in people who meditate, bottom row, than in people who don’t meditate.
Health and Medical News and Resources 