Long-Term Overtreatment with Anti-Clotting/Antiplatelet Drug Combo May Raise Risk of Dementia

(American Heart Association) Long-term overtreatment with the anti-clotting drug warfarin, combined with antiplatelet therapy with aspirin or clopidigrel to prevent stroke, may raise the risk of dementia in people with atrial fibrillation, according to research presented at the American Heart Association’s Scientific Sessions 2014.

Atrial fibrillation is a common heart rhythm abnormality that raises the risk of stroke and all common forms of dementia. The mechanisms behind the association of atrial fibrillation and dementia are unknown.

“The dual drug regimen is often used to prevent strokes in people with coronary artery disease or peripheral vascular disease, but we have to consider that long-term exposure to anti-clotting drugs such as warfarin, if not well controlled, can significantly increase bleeding risk,” said T. Jared Bunch, M.D., lead author of the study and director of electrophysiology at the Intermountain Medical Center Heart Institute in Murray, Utah.

“This may result in micro bleeds in the brain that don’t cause symptoms right away, but accumulate over time raising the risk of dementia.”

Researchers studied 1,031 patients with no previous history of stroke or dementia for up to 10 years while on the drug combination. After adjusting for traditional stroke and bleeding risk factors, patients who had abnormally slow blood clotting times — International Normalized Ratio (INR) measurement above 3 — on 25 percent or more of their monitoring tests were more than twice as likely to be diagnosed with dementia than patients whose tests showed overtreatment less than 10 percent of the time. The increase is higher than what researchers found in a previous study of warfarin alone.

Patients who had abnormally slow clotting times were considered to be receiving too much medication.

Researchers previously found that atrial fibrillation patients taking warfarin were more likely to develop dementia if lab measurements of their clotting time were frequently too slow (raising the risk of bleeding) or too fast (raising the risk of blood clots). From those results they concluded that brain injury from both small bleeds and clots was important in the development of dementia in atrial fibrillation patients.

“Even at skilled centers, it’s very common to have INR outside the ideal range up to 40 percent of the time, and over the years there may be an accumulative negative impact on cognitive ability,” Bunch said.

If you’re taking warfarin and an antiplatelet drug such as aspirin or clopidgrel, check with your doctor to make sure you need one or both of the long-term antiplatelet medications, Bunch said.

“If your INRs are consistently too high, for stroke prevention your doctor may want to consider switching you to one of the newer anti-clotting drugs that is easier to regulate or a device placed into the heart that prevents clots from forming or exiting the area in the heart chamber where most clots develop in people with atrial fibrillation,” he said.

Most patients in the study were Caucasian; so researchers aren’t sure results would apply to other ethnic groups.

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Co-authors are Heidi T. May, Ph.D.; Tami L. Bair, R.N.; Victoria Jacobs, N.P.; Brian G. Crandall, M.D.; J. Peter Weiss, M.D.; Jeffrey S. Osborn, M.D.; Charles Mallendar, M.D.; John D. Day, M.D.; Jeffrey L. Anderson, M.D.; Jeffrey L. Olson, M.D.; Katie Johanning; Yenh Long, Pharm.D.; Scott M. Stevens, M.D.; and Scott C. Woller, M.D. Author disclosures are on the manuscript.

Additional Resources:

Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability.

The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www.heart.org/corporatefunding.

Note: Actual presentation is 3 p.m. CT/4 p.m. ET Sunday, Nov. 16, 2014 (South Hall A2, Core 4).

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Alzheimer’s Drug May Reduce the Urge to Binge Eat

(Boston Medical Center via Medical News Today) The Alzheimer’s drug memantine may perform double-duty helping binge eaters control their compulsion. Researchers have demonstrated that memantine, a neuroprotective drug, may reduce the addictive and impulsive behavior associated with binge eating.

The Boston University School of Medicine (BUSM) study, which appears online in Neuopsychopharmacology, also found that a specific area in the brain, the nucleus accumbens, which is responsible for addictive behaviors, facilitates the effects of memantine.

Binge-eating disorder is a prevalent illness in America, affecting more than 10 million people. It is characterized by periods of excessive uncontrolled consumption of food, followed by uncomfortable fullness and feelings of self-disgust. New evidence indicates that changes in brain chemistry reflecting the addictive nature of binge eating may parallel drug and alcohol addiction.

Using an experimental model to simulate binge-eating behavior, researchers were able to identify the area of the brain associated with binge-eating and then suppress the behavior by applying memantine directly into that area.

“We found that memantine, which blocks glutamate NMDA receptors, blocks binge eating of junk food, blocks the strength of cues associated with junk food and blocks the compulsivity associated with binge eating,” explained senior author Pietro Cottone, PhD, an associate professor of pharmacology and psychiatry at BUSM and co-director of the Laboratory of Addictive Disorders.

This research opens new avenues for binge eating treatment especially since memantine is a drug already approved for other indications.

“Individuals with binge eating disorder have a very poor quality of life and decreased lifespan. Our study gives a better understanding of the underpinning neurobiological mechanisms of the disorder,” added coauthor Valentina Sabino, PhD, assistant professor of pharmacology and psychiatry at BUSM and co-director of the Laboratory of Addictive Disorders.

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Study Says Blood Test for Brain Insulin Resistance Accurately Predicts Alzheimer’s Disease Risk

(NanoSomiX) New Technology May Be Useful in Measuring the Prognosis and Treatment of Alzheimer’s Disease.

Brain insulin resistance is an abnormality in Alzheimer’s disease that contributes to neural cell damage and can be detected by a new blood test, according to a multi-site study that was published October 23 in the online issue of The FASEB Journal, The Journal of the Federation of American Societies for Experimental Biology. The highly statistically significant findings were made possible by a novel technique the researchers developed for measuring brain insulin resistance in living patients.

The technique involves using neuron-derived exosomes in the blood to measure insulin resistance in the brain as an indication of early-onset Alzheimer’s disease (AD). This new blood test can accurately reflect development of AD up to 10 years prior to clinical onset, the study said.

Prior to this study, it had not been possible to determine the prevalence of brain insulin resistance in living patients with AD. Nor had it been possible to determine how much time normally passes between the onset of brain insulin resistance and the appearance of clinically evident signs of AD.

In healthy individuals, the central nervous system (CNS) and other bodily tissues respond to insulin with enhanced uptake of glucose, an energy source for cells. The term “insulin resistance” describes a diverse range of reduced responses to insulin in the brain and peripheral tissues. Insulin resistance causes diminished glucose uptake in similar regions of the brain in both AD and type 2 diabetes.

Brain insulin resistance is caused by low insulin receptor signaling. This deficiency is attributable to its association with abnormal amounts of two different forms of insulin receptor substrate (IRS). The extent of these abnormalities appears to increase in patients as they progress along the AD spectrum, from mild cognitive impairment (MCI) to probable AD and with further worsening of AD.

The innovative approach used in this study allowed the researchers to extract and measure phosphorylated forms of IRS from isolated neural exosomes. Exosomes are tiny membrane-encased vesicles that are excreted from cells and are present in biological fluids such as blood, cerebrospinal fluid, etc. The ability to quantify the phosphorylated forms of IRS makes it possible to evaluate insulin resistance in the central nervous system using a blood-based assay with living patients.

The lead author of the study is Dimitrios Kapogiannis, M.D., Clinical Investigator for the National Institutes of Health, in Bethesda, Md. and the Intramural Research Program, National Institute on Aging, in Baltimore, Md.

The study found that for patients with AD and type 2 diabetes, the mean levels of the two extracted phosphorylated forms of IRS and their ratio (known as the insulin resistance index) were significantly different than the values for the healthy control group.

In addition, the researchers reported that the mean level of the brain insulin resistance index for AD was significantly higher than for either type 2 diabetes or frontotemporal dementia (FTD). 100% of the patients with AD in the study were correctly classified with the researcher’s technique, as were 97.5% of patients with type 2 diabetes. Thus, AD patients can be distinguished from the control subjects by the level of brain insulin resistance as measured by the novel blood test.

“This study shows that insulin resistance is a major central nervous system metabolic abnormality in AD that contributes to neural cell damage” said Dr. Ed Goetzl, the senior author on the study and the originator of the exosome isolation technique. “As insulin resistance is a known condition in type 2 diabetes mellitus and is treatable with several classes of existing drugs, these treatments may be useful as part of a multi-agent program for AD”.

The exosome-based technology used in the study will be further developed by NanoSomiX, a sponsor of the study, to produce a commercially available blood-based assay for researchers in academia and pharmaceutical companies. The assay will provide valuable information to those that are developing drugs for AD by using a routine and cost effective approach for early identification of subjects for inclusion in clinical trials.

“This new assay measuring brain insulin resistance further strengthens our portfolio of blood-based biomarker assays for AD using neuron-derived exosomes,” said John Osth, President and CEO of NanoSomiX.

“We believe our assays will prove instrumental in identifying early-stage AD patients for entry in clinical trials and thereby help to enrich the study population. We invite pharmaceutical companies and university researchers to contact us about collaborating or partnering to generate additional data.”

NanoSomiX will also be introducing an exosome-based blood test for p-tau, a biomarker for AD that is currently detected only in cerebrospinal fluid and with PET scans, in November.

Study sites for the just-published research included:

  • Laboratory of Neurosciences, National Institute on Aging (Baltimore, Md.)
  • The Department of Neurology, University of California-San Francisco (San Francisco, Calif.)
  • Sanders-Brown Center on Aging, University of Kentucky (Lexington, Ky.)
  • The Department of Neurology, Mayo Clinic (Rochester, Minn.)
  • The Jewish Home of San Francisco (San Francisco, CA)

Resources

Alzforum: Exosomes Stand Out as Potential Blood Biomarkers

NIH Blog: NIH-supported study shows promise for blood test for Alzheimer’s disease

About NanoSomiX

NanoSomiX, Inc. is dedicated to providing insight to researchers, clinicians, patients, their families and caregivers through the detection and management of neurodegenerative disorders via easy-to- perform, blood-based assays. The company’s flagship product is the first blood assay developed for the measurement of p-tau, a biomarker that studies have shown is tightly correlated with Alzheimer’s disease (AD). NanoSomiX is also developing additional blood-based assays for the management of AD as well as targeting other disease states. All testing is performed in a CLIA-approved laboratory in Irvine, Calif. The company is headquartered in Aliso Viejo, Calif. For more information, see www.nanosomix.com.

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Vitamin B Supplements Don’t Benefit Memory, Study Finds

(American Academy of Neurology) Taking vitamin B12 and folic acid supplements may not reduce the risk of memory and thinking problems after all, according to a new study published in the November 12, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study is one of the largest to date to test long-term use of supplements and thinking and memory skills.

The study involved people with high blood levels of homocysteine, an amino acid. High levels of homocysteine have been linked to memory loss and Alzheimer’s disease.

“Since homocysteine levels can be lowered with folic acid and vitamin B12 supplements, the hope has been that taking these vitamins could also reduce the risk of memory loss and Alzheimer’s disease,” said study author Rosalie Dhonukshe-Rutten, PhD, of Wageningen University in Wageningen, the Netherlands.

Early observational studies showed there may be some benefit to thinking and memory skills in taking folic acid and vitamin B12, but the results of later randomized, controlled trials were less convincing.

For the current study, 2,919 people with an average age of 74 took either a tablet with 400 μg of folic acid and 500 μg of vitamin B12 or a placebo every day for two years. Tests of memory and thinking skills were performed at the beginning and end of the study. All of the participants had high blood levels of homocysteine.

“While the homocysteine levels decreased by more in the group taking the B vitamins than in the group taking the placebo, unfortunately there was no difference between the two groups in the scores on the thinking and memory tests,” said Dhonukshe-Rutten.

The study was supported by the Netherlands Organization for Health Research and Development, the Dutch Dairy Association, MCO Health, Netherlands Consortium Healthy Aging, Dutch Ministry of Economic Affairs, Agriculture and Innovation, Wageningen University, VU University Medical Center and Erasmus Medical Center, all based in the Netherlands.

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To learn more about brain health, please visit http://www.aan.com/patients.

The American Academy of Neurology, an association of more than 28,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy.

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November 18th is National Memory Screening Day

(Alzheimer’s Foundation of America) Memory screenings make sense for anyone concerned about memory loss or experiencing warning signs of dementia; whose family and friends have noticed changes in them; or who believe they are at risk due to a family history of Alzheimer’s disease or a related illness. Screenings also are appropriate for anyone who does not have a concern right now, but who wants to see how their memory is now and for future comparisons.

These questions might help you decide if you should be screened. If you answer “yes” to any of them, you might benefit from a memory screening.

  • Am I becoming more forgetful?
  • Do I have trouble concentrating?
  • Do I have difficulty performing familiar tasks?
  • Do I have trouble recalling words or names in conversation?
  • Do I sometimes forget where I am or where I am going?
  • Have family or friends told me that I am repeating questions or saying the same thing over and over again?
  • Am I misplacing things more often?
  • Have I become lost when walking or driving?
  • Have my family or friends noticed changes in my mood, behavior, personality, or desire to do things?

National Memory Screening Process

A memory screening is a simple and safe evaluation tool that checks memory and other thinking skills. It can indicate whether an additional check up by a qualified healthcare professional is needed.

  • Various types of qualified healthcare professionals provide memory screenings, including social workers, pharmacists, physician assistants, nurse practitioners, psychologists and physicians.
  • The face-to-face screening takes place in a private setting; only the individual being tested and the screener are present.
  • A screening consists of a series of questions and/or tasks designed to test memory, language skills, thinking ability, and other intellectual functions.
  • Screening tools identified by AFA’s Memory Screening Advisory Board  include the GPCOG (General Practitioner Assessment of Cognition), MINI-COG, MIS (Memory Impairment Screen) and BAS (Brief Alzheimer’s Screening). These four tests meet accepted criteria for use as a screening instrument:  effective, easy to administer and validated by research, and AFA is able to offer the test for free for use during this event due to the generous permission of the copyright holders. AFA’s Memory Screening Advisory Board welcomes the review of other instruments for possible consideration; please e-mail info@nationalmemoryscreening.org.
  • The person who administers the screening will review the results with the person being screened, and suggest whether the person should follow up with a physician or other qualified healthcare professional for more extensive testing.
  • Results of the memory screenings are confidential. The participant will receive the screening results to bring to a healthcare professional for follow-up and/or inclusion in medical files.

Screening Sites

Click the map to find a screening site near you in the United States.

11-14-2014 10-47-05 AMClick here to search for sites in Canada.

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Diabetes Drugs May Be Best Available Treatment for Alzheimer’s Disease

(University of Lancaster) A new study, published in Neuropharmacology and conducted by academics at Lancaster University, could bring substantial improvements in the treatment of Alzheimer’s disease by using drugs currently on the market to treat type 2 diabetes. Alzheimer’s disease is the most common cause of dementia; it is predicted there will be more than 520,000 people in the UK with the disease in 2015.

medicationtabletswebThis study shows the newer drug lixisenatide and the older drug liraglutide (which are both currently used in the treatment of type 2 diabetes) have neuroprotective effects (i.e. protect neurons from injury or degeneration) in a mouse model of Alzheimer’s disease.

These drugs are more effective than anything currently available for the treatment of this neurodegenerative disease. Furthermore, the drug makers were unaware of the two drugs’ incredibly valuable side effects; their neuroprotective qualities.

Professor Christian Holscher, the Lancaster University academic leading this study, said:

“These are very exciting results. There are no drugs on the market for Alzheimer’s disease that actually treat the disease, all we currently have are two types of drugs that mask the symptoms for a while. Lixisenatide and liraglutide offer a real improvement by treating the basis of the disease and, therefore, preventing degeneration.”

Professor Holscher has, with other scientists from Lancaster University, founded the charity Alzheimer’s and Parkinson’s Trust NorthWest in order fund this research. He adds:

“We urgently need funding to conduct the necessary clinical trials, some of which are currently ongoing. The results of which could bring about a transformation in the treatment of Alzheimer’s disease in the very near future, as the drugs we are using in our studies have already been licenced for human use and are on the market.”

Background to Alzheimer’s disease and how the drugs work:

Impaired insulin has been linked to cerebral degenerative processes in type 2 diabetes and Alzheimer’s disease. Insulin desensitisation has also been observed in the Alzheimer’s disease brain. The desensitisation could play a role in the development of neurodegenerative disorders as insulin is a growth factor with neuroprotective properties.

Growth factor signalling has been shown to be impaired in the brains of Alzheimer’s disease patients. The deletion of the GLP-1 (a growth factor) receptor impairs learning and signal transmission in the brain, therefore treatment with GLP-1 receptor agonists (such as lixisenatide and liraglutide) has the potential to facilitate the repair in the brain and could have beneficial effects in patients with Alzheimer’s disease.

The study used APP/PS1 mice, which are transgenic mice that express human genes that cause Alzheimer’s. Those genes have been found in people who have a form of Alzheimer’s that can be inherited. Aged transgenic mice in the advanced stages of neurodegeneration were treated. As part of the study, researchers observed mice as they carried out a number of memory tasks and recorded neuronal communication in the hippocampus (one of the first areas of the brain to suffer damage in Alzheimer’s disease).

This study demonstrated an increase in synaptic numbers in APP/PS1 mice following chronic treatment with GLP-1 receptor agonists (such as lixisenatide or liraglutide). Synapses are of vital importance for communication between neurons and in Alzheimer’s disease there is considerable synapse loss.

Following chronic drug treatment, it was found that synapse numbers were not only normalised but synapses are kept functioning, ensuring that neurons were still able to communicate information. Furthermore, memory formation is normalised and protected from the detrimental effects of amyloid protein plaques in the brain, which is one of the hallmarks of Alzheimer’s disease.

Interestingly, the research also demonstrated that lower doses were just as effective as the higher doses of both drugs administered, suggesting that doses to treat type 2 diabetes may be unnecessarily high to treat neurodegenerative diseases.

Clinical trials using liraglutide are currently taking place; the results of which are expected to be available for review next year. As lixisenatide has proved to be the more successful drug in this study, researchers are currently trying to raise the funds to run clinical trials investigating its effectiveness in the treatment of Alzheimer’s disease.

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New Targets, Test to Develop Treatments for Memory Disorder

(Medical News Today) In a pair of related studies, scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified a number of new therapeutic targets for memory disorders and have developed a new screening test to uncover compounds that may one day work against those disorders.

The two studies, one published in the journal Proceedings of the National Academy of Sciences (PNAS), the other in the journal ASSAY and Drug Development Technologies, could lead new approaches to some of the most problematic diseases facing a rapidly aging world population, including Alzheimer’s and Huntington’s diseases and dementia.

“We are actively looking at molecules critical to memory formation, so these two studies work in parallel,” said Sathyanarayanan V. Puthanveettil, a TSRI biologist who led both studies. “In one study, we’re reaching for a basic understanding of the process, and in the other, we’re finding new ways to identify drug candidates so that we can cure these diseases.”

Unlocking the ‘Synaptic Proteome’

The PNAS study is one of the first detailed descriptions of the proteins that are transported to the synapses, which as a group are called the “synaptic proteome.” Synapses are the part of a nerve cell (neuron) that passes electrochemical signals to other cells during functions such as memory storage. This new approach has the potential to advance our understanding of how synapses work, how their composition changes with learning and how brain diseases might affect them.

“We know these molecules function in the synapse, and if we can regulate their function there may be some very good therapeutic opportunities there,” Puthanveettil said.

The study focuses on kinesin, a molecular motor protein that plays a role in the transport of other proteins throughout a cell.

Analyzing three kinesin complexes, the researchers found that approximately 40 to 50 percent of the protein cargos were synaptic proteins–and that the identity and location of these kinesins determine which proteins they transport. These results reveal a previously underappreciated role of kinesins in regulating the composition of the entire synaptic proteome.

Interestingly, a bioinformatics analysis revealed the three kinesin cargo complexes examined in the study are involved in neurologic diseases. Approximately 60 cargos (out of 155) of the kinesin Kif5C are implicated in psychiatric disorders, while around 20 cargos of another kinesin Kif3A are implicated in developmental disorders.

“This shows for the first time how kinesins expressed in the same neurons can carry substantially different cargos,” said Research Associate Xin-An Liu, the first author of the study. “We can use this approach to identify what molecules may be targeted for memory and in major disorders. The next step is to find how the synaptic proteome changes in neuropsychiatric diseases.”

Toward New Drug Candidates

In the ASSAY study, Puthanveettil and his colleagues describe their new high-throughput screening test for discovering potential drug candidates based on kinesin and axonal transport for the treatment of memory disorders.

“The luminescence-based assay that we developed is highly reproducible and robust,” said Puthanveetil.

Using the approach, the team screened a compound collection and identified a number of small molecules that turned on or off activity of a human kinesin.

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New Alzheimer’s-related Memory Disorder Identified

(University of Kentucky’s Sanders-Brown Center on Aging) A multi-institutional study has defined and established criteria for a new neurological disease closely resembling Alzheimer’s disease called primary age-related tauopathy (PART). Patients with PART develop cognitive impairment that can be indistinguishable from Alzheimer’s disease, but they lack amyloid plaques. Awareness of this neurological disease will help doctors diagnose and develop more effective treatments for patients with different types of memory impairment.

The study, co-led by Peter T. Nelson, MD, PhD, of the University of Kentucky’s Sanders-Brown Center on Aging, and John F. Crary, MD, PhD, of Pathology & Neuroscience with Mount Sinai Hospital, was published in the current issue of Acta Neuoropathologica.

“To make an Alzheimer’s diagnosis you need to see two things together in a patient’s brain: amyloid plaques and structures called neurofibrillary tangles composed of a protein called tau,” said Dr. Nelson, a professor of neuropathology at the University of Kentucky’s Sanders-Brown Center on Aging. “However, autopsy studies have demonstrated that some patients have tangles but no plaques and we’ve long wondered what condition these patients had.”

Plaques in the brain, formed from the accumulation of amyloid protein, are a hallmark of Alzheimer’s disease. Until now, researchers have considered cases with only tangles to be either very early-stage Alzheimer’s or a variant of the disease in which the plaques are harder to detect. However, previous in-depth biochemical and genetic studies have failed to reveal the presence of any abnormal amyloid in these patients. Although tangle-only patients can have memory complaints, the presence of plaques is a key requirement for an Alzheimer’s diagnosis.

In the current study, investigators from the United States (including five from Sanders-Brown), Canada, Europe, and Japan came together to formalize criteria for diagnosing this new neurological disorder. The study establishes that PART is a primary tauopathy, a disease directly caused by the tau protein in tangles. Many of the neurofibrillary tangles in Alzheimer’s brain, in contrast, are thought to arise secondarily to amyloid or some other stimuli. The researchers propose that individuals who have tangles resembling those found in Alzheimer’s but have no detectable amyloid plaques should now be classified as PART.

PART is most severe in patients of advanced age, but is generally mild in younger elderly individuals. The reason for this is currently unknown, but unlike Alzheimer’s disease, in which the tangles spread throughout the brain, in PART cases the tangles are restricted mainly to structures important for memory.

It is too early to tell how common PART is, but given that tangles are nearly universal in the brains of older individuals, it might be more widespread than generally recognized. While further studies are required, new diagnostic tests using brain scans and cerebrospinal fluid biomarkers for amyloid and tau are finding surprisingly high proportions of patients (as many as 25% in some studies) with mild cognitive impairment that are positive for tau but negative for amyloid.

“Until now, PART has been difficult to treat or even study because of lack of well-defined criteria,” said Dr. Nelson. “Now that the scientific community has come to a consensus on what the key features of PART are, this will help doctors diagnose different forms of memory impairment early. These advancements will have a big impact on our ability to recognize and develop effective treatments for brain diseases seen in older persons.”

Identifying the type of neurological disorder in the early stages of disease is critical if treatment is to begin before irreparable brain damage has occurred. However, in the absence of clear criteria, different forms of neurological disorders have been hard to distinguish.

As a result, PART patients may have confounded clinical trials of amyloid-targeting drugs for Alzheimer’s disease as these treatments are unlikely to be effective against tangles. Along with the development of better biomarkers and genetic risk factors for dementia, the new diagnosis criteria will help PART patients to receive more targeted therapy and improve the accuracy of clinical trials for Alzheimer’s drugs.

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