That's amyloid beta 42, total tau and ptau to be precise. The distinction between healthy vs alzheimer's is pretty remarkable http://www.ncbi.nlm.nih.gov/pubmed/19833838
I suppose that the latest paper will be useful.
Good luck !
GWAS of longitudinal amyloid accumulation on 18F-florbetapir PET in Alzheimer’s disease implicates microglial activation gene IL1RAP
Vijay K Ramanan, Shannon L. Risacher, Kwangsik Nho, Sungeun Kim, Li Shen, Brenna C. McDonald, Karmen K. Yoder, Gary D. Hutchins, John D. West, Eileen F. Tallman, Sujuan Gao, Tatiana M. Foroud, Martin R. Farlow, Philip L. De Jager, David A. Bennett, Paul S. Aisen, Ronald C. Petersen, Clifford R. Jack Jr., Arthur W. Toga, Robert C. Green, William J. Jagust, Michael W. Weiner, Andrew J. Saykin, DOI: http://dx.doi.org/10.1093/brain/awv231 3076-3088 First published online: 12 August 2015
Vijay K Ramanan
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Shannon L. Risacher
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Kwangsik Nho
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA5 Centre for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Sungeun Kim
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA5 Centre for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Li Shen
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA5 Centre for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Brenna C. McDonald
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA6 Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Karmen K. Yoder
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Gary D. Hutchins
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA
John D. West
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Eileen F. Tallman
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Sujuan Gao
4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA7 Department of Biostatistics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Tatiana M. Foroud
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA5 Centre for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Martin R. Farlow
4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA6 Department of Neurology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Philip L. De Jager
8 Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Brigham and Women’s Hospital, Boston, MA 02115, USA9 Departments of Neurology and Psychiatry, Harvard Medical School, Boston, MA 02115, USA10 Program in Medical and Population Genetics, Broad Institute, Cambridge, MA 02142, USA
David A. Bennett
11 Rush Alzheimer’s Disease Centre, Rush University Medical Centre, Chicago, IL 60612, USA
Paul S. Aisen
12 University of Southern California Alzheimer's Therapeutic Research Institute, San Diego, CA 92121, USA
Ronald C. Petersen
13 Department of Neurology, Mayo Clinic Minnesota, Rochester, MN 55905, USA
Clifford R. Jack Jr.
14 Department of Radiology, Mayo Clinic Minnesota, Rochester, MN 55905, USA
Arthur W. Toga
15 Laboratory of NeuroImaging, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
Robert C. Green
16 Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA
William J. Jagust
17 Department of Neurology, University of California, Berkeley, CA 94720, USA
Michael W. Weiner
18 Departments of Radiology, Medicine, and Psychiatry, University of California-San Francisco, San Francisco, CA 94143, USA19 Department of Veterans Affairs Medical Centre, San Francisco, CA 94121, USA
Andrew J. Saykin
1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA1 Centre for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN 46202, USA4 Indiana Alzheimer Disease Centre, Indiana University School of Medicine, Indianapolis, IN 46202, USA5 Centre for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN 46202, USA
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Summary
Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease. To identify genes influencing Alzheimer’s disease pathogenesis, we performed a genome-wide association study of longitudinal change in brain amyloid burden measured by 18F-florbetapir PET. A novel association with higher rates of amyloid accumulation independent from APOE (apolipoprotein E) ε4 status was identified in IL1RAP (interleukin-1 receptor accessory protein; rs12053868-G; P = 1.38 × 10−9) and was validated by deep sequencing. IL1RAP rs12053868-G carriers were more likely to progress from mild cognitive impairment to Alzheimer’s disease and exhibited greater longitudinal temporal cortex atrophy on MRI. In independent cohorts rs12053868-G was associated with accelerated cognitive decline and lower cortical 11C-PBR28 PET signal, a marker of microglial activation. These results suggest a crucial role of activated microglia in limiting amyloid accumulation and nominate the IL-1/IL1RAP pathway as a potential target for modulating this process.
I am sending to your attention updated information on the matter.
Telomere Length Shortening and Alzheimer Disease—A Mendelian Randomization StudyYiqiang Zhan, MD1; Ci Song, PhD1; Robert Karlsson, PhD1; Annika Tillander, PhD1; Chandra A. Reynolds, PhD2; Nancy L. Pedersen, PhD1; Sara Hägg, PhD1
[+-] Author Affiliations 1Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
2Department of Psychology, University of California, Riverside
JAMA Neurol. 2015;72(10):1202-1203. doi:10.1001/jamaneurol.2015.1513.
The latest tests
Two studies explore potential new blood tests for Alzheimer's disease
Published on November 10, 2015 at 1:25 AM · No Comments
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There is increasing evidence that the brain changes of Alzheimer's disease begin decades before memory and thinking problems occur, prompting the need for better methods of early detection for this progressive, fatal brain disease. Consequently, there is a growing school of thought that the most effective future Alzheimer's drug therapies will be administered to those who are at high risk of the disease before cognitive symptoms appear.
To bolster development of a simple, inexpensive, noninvasive test that can detect the risk of Alzheimer's disease, the Alzheimer's Association, the Crnic Institute for Down Syndrome, and the Global Down Syndrome Foundation ("Global") are funding two studies of potential new blood tests for Alzheimer's, including one that uses just one drop of blood:
One study will evaluate whether examining changes in ribonucleic acid (RNA) found in one drop of blood can accurately identify people who will develop Alzheimer's in individuals with Down syndrome who are at high risk for the disease. The study is being led by Marwan Sabbagh, M.D., Director of the Alzheimer's and Memory Disorders Division at the Barrow Neurological Institute in Phoenix, and Matt Huentelman, Ph.D., Associate Professor in the Neurogenomics Division Unit at the Translational Genomics Research Institute in Phoenix.
Another study will test whether a specific set of blood proteins can identify who is at risk for developing Alzheimer's in a unique, high -risk population, individuals with Down syndrome. The study is being led by Nicole Schupf, Ph.D., M.P.H., Dr.Ph.H., Professor of Epidemiology at Columbia University Medical Center in New York City, and Sid O'Bryant, Ph.D., Director of the Center for Alzheimer's and Neurodegenerative Disease Research at the University of North Texas Health Science Center in Fort Worth.
"Prevention of Alzheimer's dementia may be more effective and easily achieved than attempting to treat the disease once symptoms already exist and irreversible damage to the brain has already occurred," says Dean Hartley, Ph.D., Director of Science Initiatives for the Alzheimer's Association. "For this approach to be successful, we must be able to simply and accurately assess risk early in the disease process. The Alzheimer's Association and the Global Down Syndrome Foundation hope that these two exciting projects drive that effort forward."
"Autopsy is still the only way to definitively diagnose Alzheimer's disease," said Michelle Sie Whitten, President and CEO of the Global Down Syndrome Foundation. "If these researchers are successful we will be one step closer to catching Alzheimer's in its early stages and hopefully then be able to treat people with the disease earlier and actually prevent dementia from occurring, when new treatment options become available."
The grant awards are part of $1 million in new funding for Down syndrome-related Alzheimer's disease research. Four projects will receive $250,000 each through the joint funding effort.
Nearly all adults with Down syndrome begin developing the brain changes of Alzheimer's in their 30s. By age 55 or 60, it is estimated 55-70% will develop dementia. Because people with Down syndrome are at high risk for Alzheimer's, answers to important research questions about the disease may be developed more quickly in this population than by studying people with sporadic, late-onset Alzheimer's, where symptoms appear most often after age 65 - and in many cases not until the 70s or 80s.
"It used to be common for individuals with Down syndrome to die in their 30s, but because of medical advances they are now regularly living into their 50s and 60s. The irony is that they are now facing dementia due to Alzheimer's disease," says Huntington Potter, Ph.D., Director of Alzheimer's Research at the Crnic Institute for Down Syndrome and a Professor of Neurology at the University of Colorado, Denver. "At the same time, questions about Alzheimer's may be answered more quickly by studying this disease in people with Down syndrome because of their high risk for Alzheimer's and the earlier onset. Through this approach, people with Down syndrome have the opportunity to further our understanding of Alzheimer's disease and we have the opportunity to help this population."
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Scientists are not sure exactly why individuals with Down syndrome are at high risk for Alzheimer's disease but past research shows that a gene on chromosome 21 codes for the amyloid precursor protein (APP) that gets cut into fragments that accumulate into the hallmark amyloid brain plaques of Alzheimer's. People with Down syndrome are born with an extra copy of chromosome 21.
"The hope for our study is that the identification of RNA biomarkers for Alzheimer's could be used in a non-invasive blood test that requires just one drop of blood to assess an individual's risk of developing the disease, similar to the way a person with diabetes checks their blood sugar," says Sabbagh. "If we can learn early on that a person is at risk, the goal would be to start preventative therapies immediately. This could be a game changer."
"Our research could provide new information about potential biomarkers, including protein changes detected in blood, that could more accurately and easily predict the risk for Alzheimer's disease in people with Down syndrome," says Schupf. "If successful, we believe there is a chance that these biomarkers could also be used to assess Alzheimer's risk in all groups of people."
The Alzheimer's Association is the largest nonprofit funder of Alzheimer's research, having awarded more than $350 million to over 2,300 projects since 1982. The Association currently supports more than 350 ongoing research projects in 21 countries totaling more than $82 million.
The Global Down Syndrome Foundation raises funds for the Crnic Institute for Down Syndrome to underwrite critical research benefiting people with Down syndrome. To date, $5.7 million in research grants has been given to 33 investigators.
The two other research projects the Alzheimer's Association and Global are funding through the joint grant award effort are:
A test of a potential Alzheimer's drug treatment that reduces levels of toxic protein fragments in the brain of a mouse model of Down syndrome. The project is led by William Mobley, M.D., Ph.D., Chair of the Department of Neurosciences at the University of California, San Diego (UCSD) and Executive Director of UCSD's Down Syndrome Center for Research and Treatment.
A study to determine whether a protein called Dyrk1A influences the build-up of brain proteins that lead to the formation of plaques and tangles that are key features of Alzheimer's in a mouse model of Down syndrome. Dyrk1A is created by one of the genes on chromosome 21 and is overabundant in the brains of people with Down syndrome. The study is led by Fei Liu, Ph.D., Head of Molecular Neuroscience for the Research Foundation for Mental Hygiene, Inc. at the New York State Institute for Basic Research in Staten Island.
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Alzheimer's Association
Olfactory testing uses extended to Alzheimer’s disease
Published on November 20, 2015 at 5:15 PM · No Comments
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By Eleanor McDermid, Senior medwireNews Reporter
A simple olfactory test may help to identify people at increased risk of developing Alzheimer’s disease (AD) dementia, suggest findings from a population-based study.
Olfactory dysfunction, already considered a strong risk indicator for Parkinson’s disease, significantly predicted both amnestic mild cognitive impairment (MCI) and further progression to AD dementia among 1430 cognitively normal people aged an average of 79.5 years.
Rosebud Roberts (Mayo Clinic, Rochester, Minnesota, USA) and study co-authors suggest that “odor identification tests may have use for early detection of persons at risk of cognitive outcomes.”
The latest one
A slow walking speed was associated with a higher level of brain amyloid deposits in a population of older adults at a high risk of developing dementia in a new study.
The study, published online in Neurology December 2, was conducted by a team led by Natalia del Campo, PhD, University Hospital Toulouse, France.
A Culture–Brain Link: Negative Age Stereotypes Predict Alzheimer’s Disease Biomarkers.Levy, Becca R.; Ferrucci, Luigi; Zonderman, Alan B.; Slade, Martin D.; Troncoso, Juan; Resnick, Susan M.
Psychology and Aging, Dec 7 , 2015, No Pagination Specified. http://dx.doi.org/10.1037/pag0000062
Abstract
Although negative age stereotypes have been found to predict adverse outcomes among older individuals, it was unknown whether the influence of stereotypes extends to brain changes associated with Alzheimer’s disease. To consider this possibility, we drew on dementia-free participants, in the Baltimore Longitudinal Study of Aging, whose age stereotypes were assessed decades before yearly magnetic resonance images and brain autopsies were performed. Those holding more-negative age stereotypes earlier in life had significantly steeper hippocampal-volume loss and significantly greater accumulation of neurofibrillary tangles and amyloid plaques, adjusting for relevant covariates. These findings suggest a new pathway to identifying mechanisms and potential interventions related to the pathology of Alzheimer’s disease. (PsycINFO Database Record (c) 2015 APA, all rights reserved)
A group of the Lomonosov Moscow State University scientists, together with their colleagues from the Institute of Molecular Biology, Russian Academy of Sciences and the King's College London, succeeded in sorting out the mechanism of Alzheimer's disease development and possibly distinguished its key trigger.
Scientists find tau protein as better marker of Alzheimer's disease
A buildup of plaque and dysfunctional proteins in the brain are hallmarks of Alzheimer's disease. While much Alzheimer's research has focused on accumulation of the protein amyloid beta, researchers have begun to pay closer attention to another protein, tau, long associated with this disease but not studied as thoroughly, in part, because scientists only recently have developed effective ways to image tau.
Scientists discover gene that may open new door to developing treatments for Alzheimer's diseaseScientists discover gene that may open new door to developing treatments for Alzheimer's disease
Scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have identified a gene that may provide a new starting point for developing treatments for Alzheimer's disease (AD).
The increasing use of biomarkers, such as β amyloid and tau, to diagnose Alzheimer's disease (AD) will likely lead to more accurate estimates of the true incidence and prevalence of the disease, concludes a new special report from the Alzheimer's Association (AA).
The report is included in the association's annual "2017 Alzheimer's Disease Facts and Figures" document.
AD biomarkers have the potential to facilitate earlier and more accurate diagnosis and treatment, according to the report, authored by Heather M. Snyder, PhD, senior director, medical & scientific operations, Alzheimer's Association, and colleagues.
Simple odor identification tests may help track progression of Alzheimer's disease
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August 16, 2017
Odor identification tests may help scientists track the evolution of the disease in persons at risk
By the time you start losing your memory, it`s almost too late. That`s because the damage to your brain associated with Alzheimer's disease (AD) may already have been going on for as long as twenty years. Which is why there is so much scientific interest in finding ways to detect the presence of the disease early on. Scientists now believe that simple odor identification tests may help track the progression of the disease before symptoms actually appear, particularly among those at risk.
"Despite all the research in the area, no effective treatment has yet been found for AD," says Dr. John Breitner, the director of the Centre for Studies on Prevention of Alzheimer's Disease at the Douglas Mental Health Research Centre of McGill University. He is one of the authors of the study on the subject that was recently published in the journal Neurology. "But, if we can delay the onset of symptoms by just five years, we should be able to reduce the prevalence and severity of these symptoms by more than 50%."
Bubble gum or gasoline?
Close to 300 people with an average age of 63 who are at risk of developing AD because they had a parent who had suffered from the disease, were asked to take multiple choice scratch-and-sniff tests to identify scents as varied as bubble gum, gasoline or the smell of a lemon. One hundred of them also volunteered to have regular lumbar punctures to measure the quantities of various AD-related proteins whose presence in the cerebrospinal fluid (CSF).
The researchers found that those with the most difficulty in identifying odors were those in whom other, purely biological indicators of AD, were most evident.
"This is the first time that anyone has been able to show clearly that the loss of the ability to identify smells is correlated with biological markers indicating the advance of the disease," says Marie-Elyse Lafaille-Magnan, a doctoral student at McGill and the first author on the study. "For more than 30 years, scientists have been exploring the connection between memory loss and the difficulty that patients may have in identifying different odors. This makes sense because it's known that the olfactory bulb (involved with the sense of smell) and the entorhinal cortex (involved with memory and naming of odors) are among the first brain structures first to be affected by the disease."
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A cheaper way to track progression of Alzheimer's disease
"This means that a simple smell test may potentially be able to give us information about the progression of the disease that is similar to the much more invasive and expensive tests of the cerebrospinal fluid that are currently being used," the director of research program on Aging, Cognition and Alzheimer's disease of the Douglas Institute and one of the authors on the study. "However, problems identifying smells may be indicative of other medical conditions apart from AD and so should not be substituted for the current tests."
The researchers caution more that far more work needs to be done to see how changes in a person's ability to identify smells over time relates to the progression of the disease itself. For the time being, smell tests are simply one more avenue to explore as researchers look for ways to identify the disease before the symptoms actually begin to appear.
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https://www.mcgill.ca/newsroom/channels/news/could-olfactory-loss-point-alzheimers-disease-269504
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