The Silence of Doctors Around Alzheimer’s

“A fate worse than death,” my colleague muttered to me as we examined an elderly man admitted to the hospital with severe dementia.

From his medical chart we knew that the patient had been an accomplished sculptor and intellectual contrarian. He’d taught classes at a prestigious art school, and his work was exhibited across Europe and the United States. To see him now, with hardly a sliver of his personality left, encumbered with physical injustices you wouldn’t wish upon your worst enemy, was beyond heartrending.

Danielle Ofri, M.D.
Joon Park Danielle Ofri, M.D.

There was something almost shameful in bearing witness to a fellow human being’s profound indignities. I was embarrassed for him, for how embarrassed he would likely be, if his former self could see his current self. That his current self lacked the capacity to be aware of his state offered little comfort.

My colleague and I ducked out of the room in silence, lost in our own private stew of unease, wincing at our unspoken keenness to move on to other patients.

Dementia is not something we doctors talk much about. We all have many patients with dementia — and more every year — but we never seem to chat about it the way we discuss kidney disease or cancer treatment. We may talk about the difficulties of obesity or emphysema, but never about dementia.

Why the silence? It certainly isn’t that dementia is rare. Alzheimer’s disease, the most common form of dementia, is ranked as the sixth leading cause of death in the United States, thoughrecent analyses suggest that it might actually be the third.  Even if we don’t specialize in geriatrics, the aging of the general population brings dementia into the offices of every medical field, save pediatrics.

Perhaps it’s the invisibility of the illness, especially in its earlier stages. Most medical visits are crowded with the exigencies of the more clinically obvious illnesses — heart disease, diabetes, hypertension — that we doctors may miss the subtle signs of dementia.

I suspect, though, that our reticence stems from deeper issues. All the top 10 killers in America are potentially preventable, or at least modifiable — all except dementia. The medical field takes rightful pride on the progress that’s been made against heart disease, diabetes, strokes. We have tests to screen for many cancers, and treatments that prolong life. Even suicides and accidental deaths can be amenable to prevention.

But there’s nothing, really, that we can do about dementia. There aren’t any screening tests that can pick up the disease before symptoms appear. And even if there were, there aren’t any treatments that make a substantial difference.

For doctors, this is profoundly frustrating. No wonder dementia gets pushed onto the back burner. In the dishearteningly limited time of a medical visit, we’re forced to focus on the diseases we can treat.

But I think that our silence on dementia is more than that. For doctors, cognitive currency is our only currency. The idea of the mind vanishing is more petrifying than much of the bodily devastation we are privy to. The loss of intellectual capacity — not to mention personality and the ability to care for oneself — taps into an existential fear that we prefer to overlook.

I thought about this as I read a recent issue of the journal Health Affairs devoted to Alzheimer’s — nearly 200 pages that exhaustively explored the diagnosis and treatment of the disease, the experience of patients and caregivers, the mammoth burden assumed by spouses and adult children of patients. The profusion of commentary and research results and task force recommendations was an embarrassingly stark contrast to the relative silence on the clinical front.

This is not the first disease in which the clinicians have trailed the researchers, the families and the activists. The all-too-recent history of AIDS is another example. The parallels of doctors’ own discomforts and often willful ignorance easy to see.

In both cases, the actions of doctors — or lack thereof —can be only partly attributed to the practical difficulties of diagnosis and treatment. Mixed in are the existential and emotional aspects of ourselves we prefer to ignore and often remain wholly unaware of.

Most doctors are required to get recertification every 10 years, to undergo a battery of tests and training courses to keep us up to date and to identify shortfalls in our medical skills. We don’t, however, do any periodic checks on our inner selves, to uncover any lapses in our emotional core that might affect the care of our patients.

Just because the diagnosis of dementia can be difficult and treatments frustratingly limited doesn’t mean we can shy away from this disease. We need to face down our own uneasiness, confront our own disconcerting reactions, so that we may be there in full for our patients, their families and, indeed, ourselves.

Danielle Ofri is an associate professor of medicine at New York University and Bellevue Hospital. She is the editor of the Bellevue Literary Review and the author of “What Doctors Feel: How Emotions Affect the Practice of Medicine.”

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Measuring Cognitive Change in Subjects With Prodromal Alzheimer’s Disease


Objective: To investigate the sensitivity of a large set of neuropsychological tests to detect cognitive changes due to prodromal Alzheimer’s disease(AD); to compare their metrological properties in order to select a restricted number of these tests for the longitudinal follow-up of subjects with prodromal AD.

Participants: 212 patients with mild cognitive impairment were tested at baseline by a standardised neuropsychological battery, which included: the Free and Cued Selective Reminding test (FCSRT), the Benton Visual Retention test, the Deno100, verbal fluency, a serial digit learning test, the double task of Baddeley, the Wechsler Adult Intelligence Scale (WAIS) similarities, the Trail-Making Test and the WAIS digit symbol test. Patients were monitored every 6 months for up to 3 years in order to identify those who converted to AD (retrospectively classified as prodromal AD). Statistical analyses were performed using a nonlinear multivariate mixed model involving a latent process. This model assumes that the psychometric tests are nonlinear transformations of a common latent cognitive process, and it captures the metrological properties of tests.

Results: 57 patients converted to AD. The most sensitive tests in the detection of cognitive changes due to prodromal AD were the FCSRT, the semantic verbal fluency and the Deno100. Some tests exhibited a higher sensitivity to cognitive changes for subjects with high levels of cognition, such as the free recall, delayed free recall scores of the FCSRT and the semantic verbal fluency, whereas others showed a higher sensitivity at low levels of cognition, such as the total recall score of the FCSRT.

Conclusions: Tests used for the follow-up of prodromal AD subjects should be chosen among those that actually decline in this stage of the disease and should be selected according to the subject’s initial scores.

Read the full article here.

By Medscape.

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Aerobic Exercise Preserves Cognition in Nondemented Elderly

PHILADELPHIA — Continuous long-term aerobic activity has a protective effect on cognitive status and psychomotor speed in nondemented elderly, a new study has found.

“We recommend daily low-impact aerobic physical activity in older people who are able to do this type of exercise,” said lead researcher Manuel Seijo-Martinez, MD, Neurology Hospital do Salnes Pontevedra, Spain.

Dr. Seijo-Martinez presented the findings here at the American Academy of Neurology (AAN) 66th Annual Meeting.

Continuous Cycling

The analysis included 39 older individuals who were in geriatric institutions. Of these, 22 patients (8 women and 14 men; mean age, 77.94 years) had been randomly assigned to the exercise group and 17 patients (7 women and 10 men; mean age, 83.59 years) to a control group.

Researchers had originally recruited close to 500 participants, but most did not complete the study because of death or unwillingness or physical inability to carry out the continued aerobic activity, said Dr. Seijo-Martinez.

Patients in the experimental group completed at least 15 minutes of aerobic activity in the form of continuous stationary cycling every day for 15 months. The mean weekly exercise duration in this group was 134.21 minutes, or roughly 18 minutes a day.

Those in the control group carried out nonphysical activities, such as reading and playing cards.

Researchers assessed cognition using 3 tests:

  • The MEC, which is the Spanish version of the Mini-Mental State Examination but includes 3 items that analyze executive function; thus, it is “a little bit more complete,” according to Dr. Seijo-Martinez. (The cutoff score for dementia on this test is 24.)

  • The Fuld Object Memory Evaluation (FOME)

  • The Symbol Digit Modality Test (SDMT), which measures psychomotor speed and attention

The study showed that compared with the control group, the exercise group had improved cognitive status according to the MEC score (P = .037).

“There was a statistically significant worsening in the control group in terms of global cognition; however, the experimental group improved,” said Dr. Seijo-Martinez.

The exercise group, which initially did worse than the control group on the SDMT, improved significantly in the assessment of psychomotor speed (P = .011).

There was no significant difference between the groups on the FOME test of memory and learning, said Dr. Seijo-Martinez.

“We conclude that the practice of continuous long-term aerobic physical exercise seems to have a neuroprotective effect on cognitive status and psychomotor speed in elderly nondemented individuals,” said Dr. Seijo-Martinez.

The research group is planning a large study using genetic markers and MRI to measure hippocampal volume in the same nondemented population of older patients who exercise, said Dr. Seijo-Martinez.

He and his research colleagues have collected data on the effect of daily aerobic activity on older persons with mild cognitive impairment (MCI) and dementia. Although the results are yet to be presented, Dr. Seijo-Martinez said that it looks like an exercise intervention has a positive cognitive benefit in these patients.

“Maybe it won’t reverse MCI, but it might help maintain cognition or delay the start of dementia.”

Greatest Impact

Invited to comment on this new research, Maria Carrillo, PhD, vice president, medical and scientific relations, Alzheimer’s Association, said that regular physical activity, including exercise, may prove to be a beneficial strategy to lower the risk for Alzheimer’s disease and vascular dementia.

“Physical activity may have its greatest impact on brain health through its positive effects on heart health,” she told Medscape Medical News. “Some evidence suggests physical activity may directly benefit brain cells by increasing blood and oxygen flow. Because of the known cardiovascular benefits, a medically approved exercise program is a valuable part of any overall wellness plan.”

Growing evidence shows that physical activity doesn’t have to be strenuous or even require a major time commitment, added Dr. Carrillo. “It’s most effective when done regularly, and in combination with a brain-healthy diet, mental activity and social interaction.”

At this point, more research is needed, especially in large, diverse populations, to find out exactly what types of physical activity, and in what amounts, may be specifically beneficial against Alzheimer’s disease and other dementias, she added.

American Academy of Neurology (AAN) 66th Annual Meeting. Abstract P1.004. Presented April 28, 2014.

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Type 2 Diabetes May Shrink the Brain, Study Suggests


TUESDAY, April 29, 2014 (HealthDay News) — People with type 2 diabetes may lose more brain volume than is expected as they age, new research indicates.

Surprisingly, this shrinkage doesn’t appear to be linked to the damaging effect of diabetes on tiny blood vessels in the brain, but instead by how the brain handles excess sugar, the researchers noted.

“We have known for a long time that diabetes is not good for the brain,” said lead researcher Dr. R. Nick Bryan, a professor of radiology at the University of Pennsylvania’s Perleman School of Medicine in Philadelphia.

Diabetes is associated with an increased risk for stroke and dementia, he said. Until now, doctors have thought these risks were likely related to blood vessel damage related to diabetes.

“But our study suggests that there is additional damage to the brain which may be more like a brain disorder such as Alzheimer’s disease,” Bryan said. “So there may be two ways diabetes affects the brain, damage to blood vessels and brain-cell degeneration.”

The brain shrinkage seen in this study may be linked with how sugar is used by the brain, Bryan said.

“It is important that patients understand the adverse effect of their disease on their brains and cooperate with their doctors who are trying to treat their diabetes and prevent the effects of diabetes on the brain and other organs,” he said.

Bryan cautioned, however, that what isn’t known from this study is if treating diabetes will prevent or slow brain shrinkage.

Nearly 26 million people in the United States have diabetes, according to the American Diabetes Association. In type 2 diabetes, the body often doesn’t use insulin efficiently, leading to an excess of both insulin and blood sugar, according to the association.

For the study, Bryan and his colleagues used MRI scans to look at the brains of 614 people with type 2 diabetes. The volunteers had diabetes for an average of about 10 years.

They found that the longer a patient had the disease, the more brain volume loss occurred, particularly in the gray matter. Gray matter includes areas of the brain involved in muscle control, seeing and hearing, memory, emotions, speech, decision-making and self-control.

In fact, for every 10 years someone had diabetes, it looked as if the brain was about two years older than the brain of someone without diabetes, according to Bryan.

It’s important to note that this study only found an association between type 2 diabetes and greater and faster brain volume loss, and it wasn’t able to prove that type 2 diabetes was the cause of the brain shrinkage.

The report was published in the April 29 online edition of Radiology.

Dr. Souhel Najjar, director of neuroscience and stroke at Staten Island University Hospital in New York City said, “Given the increasing public health burden of type 2 diabetes, the findings of this research are very important as they link diabetes directly to brain atrophy, underscoring the importance of primary prevention and early management of diabetes in reducing the burden of dementia, particularly in older population.”

This brain loss may lead to an earlier onset of dementia, another expert noted.

Dr. Sam Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York City, said, “This is a very timely paper. There is a lot of interest and a lot of confusion about the mental impairment that accompanies type 2 diabetes.”

This study suggests that chronic high levels of insulin and sugar may be directly toxic to brain cells, he said. “This would definitely be a potential cause of dementia.”

Dr. Spyros Mezitis, an endocrinologist at Lenox Hill Hospital in New York City, said that the brain shrinkage also might be due to low blood sugar, which is a common problem for people with diabetes and can be as damaging as high blood sugar.

“Diabetes over time also affects the brain, and can lead to thinking and memory problems like Alzheimer’s disease. We need to control diabetes as soon as possible so that patients don’t have brain problems,” Mezitis said.

More information

For more information on type 2 diabetes, visit the American Diabetes Association.

SOURCES: R. Nick Bryan, M.D., Ph.D., professor, radiology, Perleman School of Medicine, University of Pennsylvania, Philadelphia; Sam Gandy, M.D., Ph.D., director, Center for Cognitive Health, Mount Sinai Hospital, New York City; Spyros Mezitis, M.D., endocrinologist, Lenox Hill Hospital, New York City; Souhel Najjar, M.D., director, Neuroscience and Stroke, Staten Island University Hospital, Staten Island, N.Y.; April 29, 2014, Radiology, online.

By Steven Reinberg
HealthDay Reporter

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The Alcoholic Brain, Autoimmune Epilepsy

Molecular analysis of brain tissue from alcoholics revealed numerous differences from normal controls, potentially providing a key link connecting the brain to behavior in chronic alcoholism. Also, another study connects autoimmunity to at least some cases of epilepsy, and a novel antipsychotic drug targets negative symptoms in schizophrenia.


This Is Your Brain on Alcohol for Years

Brain autopsies in 20 alcoholic individuals versus 20 matched controls revealed a spectrum of differences in protein types and concentrations that may “provide a molecular basis for some of the neuronal and behavioral abnormalities attributed to alcoholics,” according to a British-Spanish research group.

Led by Amaia Erdozain, PhD, and Wayne Carter, PhD, of the University of Nottingham in England, the researchers examined the prefrontal cortex (Brodmann area 9) in exquisite detail, using gel electrophoresis, two types of mass spectrometry, and other assays to identify and quantify proteins present in the postmortem tissue.

Key findings in the alcoholic specimens compared with controls included:

  • Thinner cytoskeletons around cell nuclei in cortical and subcortical neurons
  • Disrupted subcortical neuron patterning
  • “Dramatic” reductions in spectrin-beta II and in alpha- and beta-tubulins
  • Greater alpha-tubulin acetylation
  • Reduced proteasome activity

Not only might these molecular changes reflect or cause the clinical effects of chronic alcoholism, they may also contribute to the overall brain atrophy seen in the condition, the researchers suggested in their report, appearing online in PLoS ONE.

Limitations to the study included less-than-perfect assays for some proteins and variations among the alcoholic subjects in age, duration of alcoholism, and cumulative alcohol intake; these subjects may not be representative of alcoholics in the general population.

Autoimmune Basis for Epilepsy

Another study supports the notion that at least some cases of epilepsy have their roots in autoimmunity, and this one comes at the question from a new angle.

Analysis of U.S. insurance claims data on some 2.5 million people found that a diagnosis of epilepsy was nearly four-fold more common among those with autoimmune disorders, according to a report in JAMA Neurology.

Kenneth D. Mandl, MD, MPH, of Harvard Medical School in Boston, and colleagues, compared the presence of an epilepsy diagnosis in insurance plan members who had any of 12 autoimmune disorders listed in their records — such as psoriasis, rheumatoid arthritis, or celiac disease — versus other plan members

After adjusting for other factors, they found an odds ratio of 3.8 for an epilepsy diagnosis (95% CI 3.6-4.0) associated with any of these conditions. No one type of autoimmunity stood out as a special risk factor, the authors indicated.

But children in the sample appeared to be more susceptible than adults to epilepsy in conjunction with autoimmunity, with an odds ratio of 5.2 (95% CI 4.1-6.5).

Other studies have also suggested that epilepsy may have an autoimmune component, especially in cases that don’t respond to conventional anti-seizure medications.

For example, Italian researchers reported last year that they had found neural autoantigens in 14 of 72 patients with drug-resistant epilepsy.

And Mayo Clinic researchers said last fall that immunotherapies such as intravenous immunoglobulin or steroids may be tried in patients with treatment-refractory epilepsy, after achieving success in 18 out of 29 patients.

Mandl and colleagues noted that their study was based on claims data, which may be flawed and/or incomplete. Nevertheless, they wrote, “The potential role of autoimmunity must be given due consideration in epilepsy so that we are not overlooking a treatable cause.”

Continue reading the full article here.

By John Gever, Deputy Managing Editor, MedPage Today

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Brawn, Brains, and Grains of Truth

ImageMemetic Brawn

One would like to think that our refined brains are resistant to the brawn and brute force of fashion or fad, the percussion of repetition. But any such conviction would be the triumph of hope over experience. The most indelible warning of this vulnerability is perhaps the allegorical tale of the emperor’s new clothes,[1] but the tendency reverberates routinely through our culture with implications of far greater moment to public health than imperial nudity.

One example that springs to mind is the notion that more nutritious foods cost more. Certainly, diets made up of highly nutritious foods cost more than diets made up of highly processed junk.[2] But what about the comparison among likes: more and less nutritious breads, more and less nutritious spreads, more and less nutritious soups or nuts? Ask yourself how many times you have heard that more nutritious foods cost more, then ask yourself how many times any data were attached to the assertion.

Read the full article here:

By David L. Katz, MD, MPH – Medscape Neurology

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Green Tea’s Impact on Cognitive Function Now Visible


Green tea appears to boost memory by enhancing functional brain connectivity, a new imaging study suggests.

A study led by Stefan Borgwardt, MD, PhD, from the Department of Psychiatry, University of Basel, Switzerland, shows that drinking a green tea extract enhances memory performance, a finding that researchers suggest may have important clinical implications for the treatment of neuropsychiatric disorders, including cognitive impairment.

This is “the first evidence for the putative beneficial effect of green tea on cognitive functioning, in particular, on working memory processing at the neural system level by suggesting changes in short-term plasticity of parieto-frontal brain connections,” the investigators write.

The study was published online March 19 in Psychopharmacology.

Boosts Brain Plasticity

Several studies have suggested that green tea enhances cognitive functioning. However, until now, the neural mechanisms underlying these putative benefits have been unclear.

To determine whether green tea extract modulates effective brain connectivity during a working memory task and whether connectivity parameters are related to task performance, the investigators recruited 12 healthy male volunteers who consumed either a milk whey–based soft drink containing 27.5 grams of green tea extract or a similar drink without green tea.

Participants were given working memory tasks while undergoing functional magnetic resonance imaging (fMRI).

fMRI results showed increased connectivity between the parietal and the frontal cortex of the brain with the green tea extract, and these neuronal findings correlated positively with improvement in task performance.

“Our findings suggest that green tea might increase the short-term synaptic plasticity of the brain,” Dr. Borgwardt said in a statement.

“Modeling effective connectivity among frontal and parietal brain regions during working memory processing might help to assess the efficacy of green tea for the treatment of cognitive impairments in neuropsychiatric disorders such as dementia,” the researchers conclude.

The study was supported by grants from Rivella, which manufacturers the soft drink used in the study. The company had no role in study design, collection, analysis, interpretation of the data, writing of the report, or decision to submit for publication. The authors have disclosed no relevant financial relationships.

Psychopharmacology. Published online March 19, 2014. Full article

By Megan Brooks –

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