Early Alzheimer’s Detection Using Computerized Cognitive Screening

Ioannis Tarnanas M.Sc Senior Researcher Gerontechnology and Rehabilitation Research Group, ARTORG Centre for Biomedical Engineering, University of Bern, 3010 Bern, SwitzerlandMedicalResearch.com Interview with:
Ioannis Tarnanas M.Sc
Senior Researcher
Gerontechnology and Rehabilitation Research Group,
ARTORG Centre for Biomedical Engineering,
University of Bern, 3010 Bern, Switzerland

MedicalResearch.com: What are the main findings of the study?

Answer: We examined 75 healthy older people and 134 patients with mild cognitive impairment. Our aim was to collect neuropsychological, neurophysiological, neuroimaging and behavioural data by means of a virtual reality serious game, in order to model the profile of the patients who will progress to dementia within the next 2-4 years. We found that the prediction based on the performance at the virtual reality based computerized assessment instrument is comparable to that of more established and widely accepted biomarkers, such as ERP and MRI. This can be explained by the cognitive fidelity and richness of behavioural data collected with virtual reality based measures, which directly reflect neurocognitive processes affected at a very early stage.
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Alzheimer’s: Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Disease

Stephen Salloway, MD, MS Director of Neurology and the Memory and Aging Program, Butler Hospital Professor of Neurology and Psychiatry Warren Alpert Medical School Brown UniversityMedicalResearch.com Interview with:
Stephen Salloway, MD, MS
Director of Neurology and the Memory and Aging Program, Butler Hospital
Professor of Neurology and Psychiatry
Warren Alpert Medical School Brown University

MedicalResearch.com: What are the main findings of this study?

Dr. Salloway:  With the aging of the population, the G-8 and the US Congress have made finding new treatments for Alzheimer’s disease by 2025 a top priority.

These were the first large anti-amyloid monoclonal antibody trials. While the clinical outcomes were disappointing, we learned important new information that is already guiding new trials. These include:

  • Treating Alzheimer’s disease earlier, when amyloid plays its most critical role and brain injury is not well established.
  • Using amyloid biomarkers to focus treatment only on those with amyloid pathology.
  • Combining treatments as we do in cancer, HIV, and heart disease to maximize benefit, and
  • Finding medications that can safely reduce amyloid burden to a greater extent:


Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer’s Disease

Rachelle S. Doody, M.D., Ph.D., Ronald G. Thomas, Ph.D., Martin Farlow, M.D., Takeshi Iwatsubo, M.D., Ph.D., Bruno Vellas, M.D., Steven Joffe, M.D., M.P.H., Karl Kieburtz, M.D., M.P.H., Rema Raman, Ph.D., Xiaoying Sun, M.S., Paul S. Aisen, M.D., Eric Siemers, M.D., Hong Liu-Seifert, Ph.D., and Richard Mohs, Ph.D. for the Alzheimer’s Disease Cooperative Study Steering Committee and the Solanezumab Study Group

N Engl J Med 2014; 370:311-321
January 23, 2014
DOI: 10.1056/NEJMoa1312889

Alzheimer’s Disease: Connection with Rare Childhood Disorder

Alessandra d’Azzo PhD Department of Genetics, St Jude Children’s Research Hospital 262 Danny Thomas Place, Memphis, Tennessee 38105MedicalResearch.com Interview with:
Alessandra d’Azzo PhD
Department of Genetics, St Jude Children’s Research Hospital
262 Danny Thomas Place, Memphis, Tennessee 38105

MedicalResearch.com: What are the main findings of the study?

Dr. d’Azzo: We have discovered a connection between a rare childhood disorder and Alzheimer’s disease that usually affects older people.

The culprit is a metabolic enzyme called NEU1 that normally controls the recycling or disposal of proteins in a specific cell compartment, the lysosome.
When NEU1 is defective, children develop the severe metabolic disease, sialidosis.

Our study suggests that NEU1 also plays an important role in the development of Alzheimer’s disease. Based on this discovery, we decided to increase NEU1 enzyme activity in the brain of an Alzheimer’s disease mouse model that shows features characteristic of the human disease, namely the accumulation of toxic protein aggregates or plaques. Remarkably, we could significantly diminish the number of plaques in the brain of these mice by increasing NEU1 enzyme activity.
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Alzheimer disease: Genetic Risk Mitigated by Good Sleep

MedicalResearch.com Interview with:
Assistant Professor and Clinician Scientist
Division of Neurology, Department of Medicine
Sunnybrook Health Sciences Centre
University of Toronto

MedicalResearch.com: What are the main findings of the study?

Dr. Lim: Alzheimer disease (AD) is the result of a confluence of genetic, behavioral, and environmental risk factors.  The Apolipoprotein E (APOE) e4 allele is the most common and well established genetic risk factor for Alzheimer Disease.  10-20% of the US population carries the high risk APOE e4 allele, which confers up to a 30% lifetime risk of AD. Meanwhile, previous work had suggested that poor sleep may be a risk factor for AD and that APOE genotype and poor sleep may amplify each other’s negative cognitive effects.

We asked the question whether good sleep consolidation (i.e. sound sleep without repeated awakenings) may reduce the effect of APOE on the risk of incident AD and the burden of AD pathology.  We studied 698 individuals without dementia participating in the Rush Memory and Aging Project – a longitudinal cohort study of aging and risk factors for AD.  We measured sleep consolidation using wrist-watch like devices called actigraphs, and followed participants for up to 6 years, examining them annually for the development of AD.  Autopsies were perfumed on 201 participants who died during the follow-up period and we quantified the burden of AD pathology.

During the follow-up period, 98 participants developed AD.  As expected, carrying the APOE e4 allele was associated with a higher risk of AD, faster cognitive decline, and a higher burden of AD pathology (amyloid plaques and neurofibrillary tangles) at death. However, better sleep at baseline significantly reduced the negative impact of APOE e4 on the risk of AD, rate of cognitive decline, and burden of neurofibrillary tangle pathology.
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Alzheimer’s and Albumin-Amyloid Beta Complexes

MedicalResearch.com Interview with:
Keiichi Yamamoto, MD, PhD
Department of Geriatric Medicine and Neurology,
Osaka City University Graduate School of Medicine
Osaka, Japan.

MedicalResearch.com: What are the main findings of the study?

Answer: Aβ is normally bound to and transported by albumin in blood. We therefore hypothesized that decreased blood levels of Albumin-Aβ complexes may be associated with decreased Aβ removal from brain to blood, resulting in Aβ accumulation in the brain. This is the first study demonstrated that decreased serum level of albumin-Aβ complexes was strongly associated with a higher prevalence of Alzheimer’s disease (AD). This association was independent of age, sex, and ApoE4 allele. In addition, decreased serum level of albumin-Aβ complexes was correlated with decreased levels of Aβ42 in the CSF and increased levels of p-tau in the CSF, findings that have been shown to be associated with specific neuropathologic findings and AD progression.

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Alzheimer’s Disease: Evidence for Genetic Risk Factor

MedicalResearch.com Interview with: Steve Estus PhD

Dept. of Physiology University of Kentucky
Office: Room 332 Sanders-Brown Building
800 S. Limestone Street
Lexington, KY 40536-0230

MedicalResearch.com: What are the main findings of the study?

Answer: We report evidence for the function of a Alzheimer’s genetic  risk factor.  This protective allele of the polymorphism decreases the splicing efficiency of exon 2 in CD33, a receptor protein that regulates microglial activation.  Loss of exon 2 appears to produce a dormant CD33 protein, resulting in increased microglial phagocytosis activity.  Overall, these findings confirm and extend recent papers in Neuron and Nature Neuroscience  (discussed further in our report) that described decreased CD33 activity with the protective SNP allele.

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Degenerative Disease Research: Structural basis of kynurenine 3-monooxygenase inhibition

MedicalResearch.com eInterview: Professor Nigel S. Scrutton ScD FRSC FSB

Director Manchester Institute of Biotechnology
EPSRC Established Career Fellow |Faculty of Life Sciences | Manchester Institute of Biotechnology | University of Manchester | Manchester | M1 7DN | UK |

MedicalResearch.com: What are the main findings of your study?

Dr. Scrutton: A major breakthrough has been made by our team of researchers seeking treatments for degenerative illnesses such as Parkinson’s Disease.

We have detailed how an enzyme in the brain interacts with a drug-like lead compound directed against Huntington’s Disease (but also with major implications for Alzheimer’s and Parkinson’s diseases) to inhibit its activity. The work – which solved the molecular structure of a crucial brain enzyme called kynurenine 3-monooxygenase – opens the door to effective treatment for neurodegenerative diseases such as Huntington’s, Alzheimer’s and Parkinson’s. The main findings not only describe the molecular details of the enzyme, but also how it interacts with a lead drug compound that inhibits the natural activity of the enzyme.
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Alzheimer’s plaques in PET brain scans identify future cognitive decline

Alzheimer’s plaques in PET brain scans identify future cognitive decline

DURHAM, N.C. – Among patients with mild or no cognitive impairment, brain scans using a new radioactive dye can detect early evidence of Alzheimer’s disease that may predict future decline, according to a multi-center study led by researchers at Duke University Medical Center.

The finding is published online July 11, 2012, in the journal Neurology, the medical journal of the American Academy of Neurology. It expands on smaller studies demonstrating that early detection of tell-tale plaques could be a predictive tool to help guide care and treatment decisions for patients with Alzheimer’s disease.

“Even at a short follow-up of 18 months we can see how the presence of amyloid plaques affects cognitive function,” said P. Murali Doraiswamy, M.D., professor of psychiatry at Duke who co-led the study with R. Edward Coleman, M.D., professor of radiology at Duke . “Most people who come to the doctor with mild impairment really want to know the short-term prognosis and potential long-term effect.”

Doraiswamy said such knowledge also has some pitfalls. There is no cure for Alzheimer’s disease, which afflicts 5.4 million people in the United States and is the sixth-leading cause of death among U.S. adults. But he said numerous drugs are being investigated, and identifying earlier disease would improve research into their potential benefits and speed new discoveries, while also enhancing care and treatment of current patients.

In the Neurology study, 151 people who had enrolled in a multi-center test of a new radioactive dye called florbetapir (Amyvid) were recruited to participate in a 36-month analysis. Of those participants, 69 had normal cognitive function at the start of the study, 51 had been diagnosed with mild impairment, and 31 had Alzheimer’s dementia.

All completed cognitive tests and underwent a brain scan using Positron Emission Tomography, or PET imaging. The technology uses radioactive tracers designed to highlight specific tissue to create a three-dimensional picture of an organ or a biological function.

The dye used in the study, florbetapir, was recently approved by the U.S. Food and Drug Administration for PET imaging of the brain to estimate beta-amyloid plaque density in patients who are being evaluated for cognitive impairment. It binds to the amyloid plaques that characterize Alzheimer’s disease, providing a window into the brain to see if the plaques have formed, and how extensively.

Patients in the study were reassessed with additional cognitive exams at 18 months and 36 months. At the 18-month point, patients with mild cognitive impairment who had PET evidence of plaque at the trial’s start worsened to a great degree on cognitive tests than patients who had no evidence of plaque at the trial’s start. Twenty-nine percent of the plaque-positive patients in this group developed Alzheimer’s dementia, compared to 10 percent who started with no plaque.

Cognitively normal patients with a plaque-positive PET scan at the start of the study also showed more mental decline at 18 months compared to those who were negative for plaque.

The study additionally found that people with negative scans reversed from minimally impaired to normal more often than people with positive PET scan, suggesting test anxiety or concentration problems could have affected their initial performance.

“For the most part we have been blind about who would progress and who wouldn’t, so this approach is a step toward having a biomarker that predicts risk of decline in people who are experiencing cognitive impairment,” Doraiswamy said.

He said the study’s results provide initial data that needs to be verified by additional research. Final, 36-month data from the study has been completed and will be presented at the Alzheimer’s Association International Conference this week in Vancouver, Canada. Doraiswamy also cautioned that florbetapir is currently not approved to predict the development of dementia or other neurologic conditions and stressed that it should not be used as a screening tool in otherwise normal or minimally impaired people. Likewise, a positive scan is not necessarily diagnostic for Alzheimer’s by itself.


In addition to Doraiswamy and Coleman (who died in June), study authors included; Reisa A. Sperling and Keith A. Johnson of Massachusetts General Hospital, Boston Medical School; Eric M. Reiman of Banner Alzheimer’s Institute; Mat D. Davis of the University of Pennsylvania; Michael Grundman of Global R&D Partners and the University of California, San Diego; Marwan N. Sabbagh of Banner-Sun Health Research Institute; Carl H. Sadowsky of Nova SE University; Adam S. Fleisher of Banner Alzheimer’s Institute and UCSD; and Alan Carpenter, Christopher M. Clark (deceased), Abhinay D. Joshi, Mark A. Mintun, Daniel M. Skovronsky, and Michael J. Pontecorvo of Avid Radiopharmaceuticals.

Alzheimer's plaques in PET brain scans identify future cognitive decline

Caption: PET images using florbetapir dye to highlight beta-amyloid plaques show (A), a cognitively normal subject; (B) an amyloid-positive patient with Alzheimer’s disease; (C) a patient with mild cognitive impairment; and (D) a patient with mild cognitive impairment who progressed to dementia during the study.
Credit: Slide courtesy of the journal Neurology.

New Method May Help Detect Marker for Alzheimer’s Disease Earlier

Newswise — NEW ORLEANS – Use of a new drug to detect the beta-amyloid plaques in the brain that are hallmark signs of Alzheimer’s disease may help doctors diagnose the disease earlier, according to research that will be presented as part of the Emerging Science program (formerly known as Late-Breaking Science) at the American Academy of Neurology’s 64th Annual Meeting in New Orleans April 21 to April 28, 2012.

Currently, Alzheimer’s disease can only be definitively confirmed through the detection of amyloid plaques and/or tangles in the brain during autopsy after death or with a brain tissue biopsy. The new method uses the drug florbetaben as a tracer during a PET scan of the brain to visualize amyloid plaques during life.

In order to prove that the florbetaben PET scan detects beta-amyloid in the brain, the global phase III study directly compared brain regions in the PET scan to respective brain regions after death during autopsy.

For the study, more than 200 participants nearing death (including both participants with suspected Alzheimer’s disease and those without known dementia) and who were willing to donate their brain underwent MRI and florbetaben PET scan. The amount of plaque found in the 31 participants who reached autopsy was then compared to the results of the scans. A total of 186 brain regions from these donors were analyzed along with 60 brain regions from healthy volunteers. Based on these 246 brain regions the study found florbetaben to detect beta-amyloid with a sensitivity of 77 percent and a specificity of 94 percent.

Comparison of the visual assessment method proposed for florbetaben for clinical practice with the post mortem diagnosis revealed a sensitivity of 100 percent and a specificity of 92 percent. Sensitivity is the percentage of actual positives that are correctly identified as positive, and specificity is the percentage of negatives that are correctly identified.

“These results confirm that florbetaben is able to detect beta-amyloid plaques in the brain during life with great accuracy and is a suitable biomarker,” said study author Marwan Sabbagh, MD, director of Banner Sun Health Research Institute in Sun City, Ariz., and a Fellow of the American Academy of Neurology. “This is an easy, non-invasive way to assist an Alzheimer’s diagnosis at an early stage. Also exciting is the possibility of using florbetaben as tool in future therapeutic clinical research studies where therapy goals focus on reducing levels of beta-amyloid in the brain.”

The study was supported by Bayer Healthcare Berlin.

Blood Tests May Hold Clues to Pace of Alzheimer’s Disease Progression

Release Date: 10/03/2011

Johns Hopkins-led research suggests levels of certain fats in blood might predict rate of cognitive decline.

A team of scientists, led by Johns Hopkins researchers, say they may have found a way to predict how quickly patients with Alzheimer’s disease (AD) will lose cognitive function by looking at ratios of two fatty compounds in their blood. The finding, they say, could provide useful information to families and caregivers, and might also suggest treatment targets for this heartbreaking and incurable neurodegenerative disorder.

Past research has shown that cognitive function declines at different rates in AD patients, with roughly one-third not declining at all in five years, one-third declining at a moderate rate, and the other third declining quickly. Accurately predicting the pace of cognitive decline would help patients and caregivers better prepare and, if treatments are developed, help doctors aggressively target those whose descent into dementia is likely to be accelerated. Currently there are no predictably effective treatments that prevent, slow or stop AD, though the researchers caution that more studies need to be done before their blood fat test proves its value.

“We’re confident there’s a relationship between these lipids and AD progression, but this work is not yet ready to be used clinically,” according to Michelle Mielke, Ph.D., adjunct assistant professor of psychiatry at the Johns Hopkins University School of Medicine and lead author of an article about the work published in the Journal of Alzheimer’s Disease.

Mielke’s team analyzed data from 120 probable Alzheimer’s patients at the Alzheimer’s Disease and Memory Disorders Center at Baylor College of Medicine in Texas, measuring a variety of fats found in the patients’ blood, as well as conducting cognitive assessments during an average of 4.2 visits over 2.3 years. The researchers found that the higher the level of plasma sphingomyelins and the lower the level of ceramide — two types of fat found in cells throughout the body — the slower the progression of the dementia of Alzheimer’s disease.

Although the researchers emphasize that the link between the fats and AD is not well understood, ceramides are involved in inflammation and cell death. If there are fewer of these cell-killing ceramides circulating — which in turn may be killing off fewer important brain cells — the result may be slower disease progression, Mielke says. Meanwhile, a previous study by Mielke and her team showed that higher ceramide levels were associated with greater shrinkage of the brain’s memory center over one year in patients with mild cognitive impairment. Basic science data has also linked ceramide levels and levels of the protein amyloid beta, the accumulation of which has been tied to Alzheimer’s disease.

If the blood fat ratios do turn out to be important, Mielke says there may be ways to use this discovery to slow cognitive decline. For example, an enzyme known as sphingomyelinase metabolizes sphingomyelins into ceramides. It is possible, she says, that if a sphingomyelinase inhibitor were used to slow down the process of breaking down sphingomyelins into ceramides, the progression of the disease could be interrupted.

Though much research has been done to find ways to halt Alzheimer’s, so far the only approved therapy treats symptoms of cognitive decline in some patients for a short period of time. It does nothing to alter the course of the disease.

“And none of the other compounds in clinical trials to date are showing any benefits,” says Mielke, who is also an associate consultant in the division of epidemiology at the Mayo Clinic. “Perhaps we need to shift our focus. The answers could be in these lipids, which can be measured in the blood.”

Other Hopkins researchers contributing to this work include Norman J. Haughey, Ph.D.; Vera Venkata Ratnam Bandaru, Ph.D.; and Constantine G. Lyketsos, M.D.

Research Supports Upcoming Alzheimer’s Disease Guidelines

Reston, Va.–Two new studies published in the August issue of The Journal of Nuclear Medicine (JNM) provide insight intothe potential of positron emission tomography (PET) to differentiate between types of dementia and to identify pharmaceuticals to slow the progress of dementia. With proposed National Institute on Aging (NIA) and the Alzheimer’s Association guidelines for detecting Alzheimer’s-related brain changesexpected in September, these articles give a preview of what may be to come.

Earlier this year, the NIA and the Alzheimer’s Association released new criteria and guidelines for the diagnosis of Alzheimer’s disease. The new proposed guidelines available this fall will offer additional information regarding the development of tests to measure biological changes in the brain, blood, or spinal fluid to diagnose Alzheimer’s at an earlier stage.

Earlier diagnosis of Alzheimer’s disease is the focus of the JNM article “Amyloid Imaging with 18F-Florbetaben in Alzheimer Disease and Other Dementias.” In this study researchers compared cortical amyloid deposition using 18F-florbetaben and PET in 109 controls and subjects with mild cognitive impairment (MCI), frontotemporal lobar degeneration, dementia with Lewy bodies, vascular dementia, Parkinson’s disease and Alzheimer’s disease.

The results show that 18F-florbetaben performs with the same high accuracy as previously reported with 11C-Pittsburgh Compound B—the most specific and widely used amyloid imaging agent—for distinguishing between certain types of neurodegenerative dementia, particularly for diagnosis of Alzheimer’s disease from frontotemporal dementia.

“The difference between 11C-Pittsburgh Compound B and 18F-florbetaben is that the 18F-florbetaben has a longer half life and is more affordable, making it appropriate for clinical use,” said Christopher Rowe, MD, FRACP, one of the authors of the study.  “This distinction profoundly affects treatment and prognosis and has genetic implications for the family.”

In addition to detecting Alzheimer’s disease earlier, molecular imaging can also be used in clinical trials to help develop pharmaceuticals to prevent or delay the onset of dementia. This is particularly of importance to patients with MCI who have yet to develop Alzheimer’s disease.

“We urgently need tools for conducting drug trials for MCI more efficiently,” noted Karl Herholz, MD, lead author of the study “Evaluation of a Calibrated 18F-FDG PET Score as a Biomarker for Progression of Alzheimer’s Disease and Mild Cognitive Impairment.” He continued, “Clinical outcome parameters show large variability and little sensitivity to progression at that stage, making these trials extremely costly and cumbersome. By using imaging biomarkers as primary outcome parameters, clinical trials can be performed with smaller sample sizes or shorter trial duration without loss of study power.”

The study evaluated a predefined quantitative measure—a PET score—that was extracted automatically from 18F-FDG PET scans using a sample of controls, patients with MCI and patients with Alzheimer’s disease. The PET scores provided a much higher test-retest reliability than standard neuropsychologic test scores (Alzheimer’s Disease Assessment Scale-Cognitive and Mini-Mental State Examination) and superior strength for measuring progression, as well as a valid measurement of cognitive impairment. As such, the PET scores can be considered a valid imaging biomarker to monitor the progression of MCI to Alzheimer’s disease.

“Prevention of dementia by drugs applied at MCI stage would greatly improve quality of life for patients and reduce costs of dementia care and treatment. Thus, development of such drugs and efficient tools for testing them are extremely important,” concluded Herholz.

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks of daily living. Although treatment can slow the progression of the disease and help manage its symptoms, there is no cure for Alzheimer’s disease. The Alzheimer’s Association estimates that more five million people are currently living with the disorder.

Authors of the article “Amyloid Imaging with 18F-Florbetaben in Alzheimer Disease and Other Dementias” include: Victor Villemagne, Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia, Department of Medicine, University of Melbourne, Parkville, Victoria, Australia and The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia; Kevin Ong and Christopher Rowe, Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia and Department of Medicine, University of Melbourne, Parkville, Victoria, Australia; Rachel S. Mulligan, Svetlana Pejoska, Gareth Jones, Graeme O’Keefe, Uwe Ackerman, Henri Tochon-Danguy and J. Gordon Chan, Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia; Colin L. Masters, The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia; and Gerhard Holl, Cornelia B. Reininger, Lueder Fels, Barbara Putz and Beate Rhode, Bayer Schering Pharma, Berlin, Germany.

Authors of the article “Evaluation of a Calibrated 18F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment” include: Karl Herholz, Sarah Westwood and Cathleen Haense, Wolfson Molecular Imaging Centre, School of Cancer and Enabling Sciences, University of Manchester, Manchester, United Kingdom, and Graham Dunn, School of Community Based Medicine, University of Manchester, Manchester, United Kingdom.


Atherosclerosis linked to Dementia

American Stroke Association Scientific Statement

Statement Highlights:
• High blood pressure is related to the development of age-related vascular cognitive impairment.
• Maintaining a healthy heart may also maintain a healthy functioning brain, according to the statement.
• Screening elderly patients for heart and stroke risk factors may also identify those at risk of dementia.

DALLAS, July 21 — The same artery-clogging process (atherosclerosis) that causes heart disease can also result in age-related vascular cognitive impairments (VCI), according to a new American Heart Association/American Stroke Association scientific statement published online in Stroke: Journal of the American Heart Association.

Cognitive impairment, also known as dementia, includes difficulty with thinking, reasoning and memory, and can be caused by vascular disease, Alzheimer’s disease, a combination of both and other causes.

Atherosclerosis is a build- up of plaque in the arteries associated with elevated blood pressure, cholesterol, smoking and other risk factors. When it restricts or blocks blood flow to the brain, it is called cerebrovascular disease, which can result in vascular cognitive impairment.

Alzheimer’s disease is a progressive brain disorder that damages and destroys brain cells.
“We have learned that cerebrovascular disease and Alzheimer’s disease may work together to cause cognitive impairment and the mixed disorder may be the most common type of dementia in older persons,” said Philip B. Gorelick, M.D., M.P.H., co-chair of the writing group for the statement and director of the Center for Stroke Research at the University of Illinois College of Medicine at Chicago.

The prevalence of dementia increases with advancing age and affects about 30 percent of people over 80 years of age, costing more than $40,000 per patient annually in the United States, according to the statement authors. . .

Treating risk factors for heart disease and stroke with lifestyle changes and medical management may prevent or slow the development of dementia in some people, Gorelick said. Physical activity, healthy diet, healthy body weight, tobacco avoidance as well as blood pressure and cholesterol management could significantly help many people maintain their mental abilities as they age.

“Generally speaking, what is good for the heart is good for the brain,” Gorelick said. “Although it is not definitely proven yet, treatment or prevention of major risk factors for stroke and heart disease may prove to also preserve cognitive function with age.”

Understanding common causes of late-life cognitive impairment and dementia has advanced and many of the traditional risk factors for stroke also are risk markers for Alzheimer’s disease and vascular cognitive impairment. For example:

• Reducing high blood pressure is recommended to reduce the risk of vascular cognitive impairment. High blood pressure in mid-life may be an important risk factor for cognitive decline later in life.
• Controlling high cholesterol and abnormal blood sugar may also help reduce the risk of vascular cognitive impairment, although more study is needed to confirm the role of these interventions.
• Smoking cessation could lessen the risk of vascular cognitive impairment.
• Increasing physical exercise, consuming a moderate level of alcohol (i.e., up to 2 drinks for men and 1 drink for non-pregnant women) for those who currently consume alcohol; and maintaining a healthy weight may also lessen the risk of VCI, but more study is needed to confirm usefulness.
• Taking B vitamins or anti-oxidant supplements, however, does not prevent vascular cognitive impairment, heart disease or stroke.

Identifying people at risk for cognitive impairment is a promising strategy for preventing or postponing dementia and for public health cost savings, the writers said. “We encourage clinicians to use screening tools to detect cognitive impairment in their older patients and continue to treat vascular risks according to nationally- or regionally-accepted guidelines.”
Vascular cognitive impairment is most obvious after a stroke, but there could be cognitive repercussions from small strokes, microbleeds or areas of diminished blood flow in the brain that cause no obvious neurological symptoms, according to the statement.

In many cases, the risk factors for vascular cognitive impairment are the same as for stroke, including high blood pressure, high cholesterol, abnormalities in heart rhythm and diabetes.
The American Academy of Neurology and the Alzheimer’s Association have endorsed the statement.

Other members of the writing group include: Angelo Scuteri, co-chair, M.D., Ph.D.; David Bennett, M.D.; Sandra E. Black, M.D.; Charles DeCarli, M.D.; Helena C. Chui, M.D.; Steven M. Greenberg, M.D., Ph.D.; Randall T. Higashida, M.D.; Costantino Iadecola, M.D.; Lenore J. Launer, M.D.; Stephane Laurent, M.D.; Oscar L. Lopez, M.D.; David Nyenhuis, Ph.D.; Ronald C. Petersen, M.D., Ph.D.; Julie A. Schneider, M.D.; Christophe Tzourio, M.D., Ph.D.; Donna K. Arnett, Ph.D.; Ruth Lindquist, Ph.D., R.N.; Peter M. Nilsson, M.D., Ph.D.; Gustavo C. Roman, M.D.; Frank W. Sellke, M.D.; and Sudha Seshadri, M.D. Author disclosures are on the manuscript.

NR11-1102 (Stroke/Gorelick)

Additional resources:
• For information about emotional and behavioral challenges after stroke, visit www.strokeassociation.org/LifeAfterStroke