AC Immune Announces First Positive Cognitive Results for a Tau-Targeting Monoclonal Antibody in Alzheimer’s Disease

This means that your doctor is responsible to identify your Alzheimers early so you can be treated with this when it is finally approved. What is your doctor's protocol on dementia testing? 

AC Immune Announces First Positive Cognitive Results for a Tau-Targeting Monoclonal Antibody in Alzheimer’s Disease

Top-line data from Lauriet Phase 2 trial of semorinemab in mild-to-moderate AD shows a statistically significant reduction on one of two co-primary endpoints, ADAS-Cog11

First evidence of clinical activity in tau-targeting monoclonal antibody in MMSE 16-21 (mild-to-moderate) AD population

Partner Genentech to continue open label portion of the study and plans to submit top line results for presentation at November CTAD 2021 congress

LAUSANNE, Switzerland, Aug. 31, 2021 (GLOBE NEWSWIRE) -- AC Immune SA (NASDAQ: ACIU), a clinical-stage biopharmaceutical company pioneering precision medicine for neurodegenerative diseases, today announced that Genentech, a member of the Roche Group, has informed the Company that Lauriet, a placebo-controlled Phase 2 study evaluating the safety and efficacy of the investigational anti-tau monoclonal antibody, semorinemab, in mild-to-moderate Alzheimer’s disease (AD), met one of its co-primary endpoints, ADAS-Cog11. The second co-primary endpoint, ADCS-ADL, was not met. Safety data showed that semorinemab is well tolerated with an acceptable safety profile and no unanticipated safety signals.

Semorinemab demonstrated a statistically significant reduction in cognitive decline from baseline by 43.6% compared to placebo (p<0.0025) as measured by the Alzheimer’s Disease Assessment Scale, Cognitive Subscale, 11-item Version (ADAS-Cog11) at week 49 in people with mild-to-moderate AD (i.e., Mini-Mental State Examination (MMSE) 16-21). There was no effect on the other co-primary endpoint of reducing the rate of functional decline from baseline as measured by the Alzheimer’s Disease Cooperative Study-Activities of Daily Living (ADCS-ADL) or secondary efficacy endpoints for the Mini-Mental State Examination (MMSE) or the Clinical Dementia Rating-Sum of Boxes (CDR-SB). The safety was consistent with previous clinical data reported.

Genentech has reported that the open label portion of the study will continue as planned. Further analyses are ongoing, and top-line data will be submitted for presentation at the CTAD conference (Clinical Trials on Alzheimer's Disease conference) in November.

Prof. Andrea Pfeifer, CEO of AC Immune SA, commented: “The top line results of the Lauriet Phase 2 clinical trial of semorinemab are remarkable in that it is the first time we have seen a therapeutic effect by a monoclonal anti-Tau antibody therapy. We also are excited by the fact that this is the first time a monoclonal antibody has had a therapeutic impact on cognition in the mild-to-moderate AD patient population. Nevertheless, despite these interesting results, we are still cautious about what this may mean for patients as there was not an impact on the rate of functional decline or other efficacy endpoints. With that said, AD is a slow-moving chronic disease, and this small trial was relatively short, 49 weeks; so, the data from the open-label extension may be important in elucidating the potential of semorinemab in this patient population. Scientifically, these data are encouraging for the therapeutic strategies targeting Tau. We look forward to additional data from our other clinical-stage Tau programs: Tau vaccine ACI-35, partnered with Janssen; and the small molecule Morphomer^® Tau aggregation inhibitor, partnered with Eli Lilly.”

About the Lauriet study
Lauriet is a double-blind, placebo-controlled, randomized Phase II trial assessing semorinemab, an investigational anti-tau monoclonal antibody, compared to placebo in 272 adult participants with mild-to-moderate AD across 43 study centers globally. The primary endpoints of the study evaluated the change from baseline at week 49 in cognition as measured by the Alzheimer’s Disease Assessment Scale, Cognitive Subscale, 11-Item Version (ADAS-Cog11) and the change from baseline in activities of daily living as measured by the Alzheimer’s Disease Cooperative Study-Activities of Daily Living (ADCS-ADL) scale. Secondary endpoints evaluated cognitive and functional measures including changes from baseline as measured by the Clinical Dementia Rating-Sum of Boxes (CDR-SB) and the Mini-Mental State Examination (MMSE). The Lauriet open label extension is ongoing. For more information, visit ClinicalTrials.gov (NCT03828747).

About semorinemab
Semorinemab is an investigational monoclonal anti-tau antibody that targets the N-terminal portion of the tau protein, and is designed to bind to tau and slow its spread between neurons. In tauopathies such as AD, tau misfolds and forms tangles, which cause cell damage and ultimately neuronal death. It is hypothesized that abnormal tau protein then spreads between neurons, gradually involving more areas of the brain, and leading to clinical disease progression. Tau-targeting antibody therapies are designed to slow or stop this process of tau spread. Semorinemab is being developed by Genentech and was identified in collaboration with AC Immune (Nasdaq: ACIU, Lausanne, Switzerland). Semorinemab has been studied in two Phase 2 studies – Lauriet in mild-to-moderate AD and Tauriel in early (prodromal-to-mild) AD, where the primary efficacy endpoint was not met.

About AC Immune SA 
AC Immune SA is clinical-stage biopharmaceutical company that aims to become a global leader in precision medicine for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and NeuroOrphan indications driven by misfolded proteins. The Company’s two clinically validated technology platforms, SupraAntigen^® and Morphomer^®, fuel its broad and diversified pipeline of first- and best-in-class assets, which currently features ten therapeutic and three diagnostic candidates, six of which are currently in clinical trials. AC Immune has a strong track record of securing strategic partnerships with leading global pharmaceutical companies including Genentech, a member of the Roche Group, Eli Lilly and Company, and Janssen Pharmaceuticals, Inc., resulting in substantial non-dilutive funding to advance its proprietary programs and over $3 billion in potential milestone payments.

SupraAntigen^® is a registered trademark of AC Immune SA in the following territories: AU, EU, CH, GB, JP and RU. Morphomer^® is a registered trademark of AC Immune SA in CN, CH, GB, JP, and NO.

For further information, please contact:

Media Relations Saoyuth Nidh AC Immune Phone : +41 21 345 91 34 Email: saoyuth.nidh@acimmune.com	Investor Relations Yves Kremer, Ph.D. AC Immune Phone : +41 21 345 91 90 Email: yves.kremer@acimmune.com
U.S. Media Katie Gallagher LaVoie Health Science Phone: +1 617 792 3937 Email: kgallagher@lavoiehealthscience.com	U.S. Investors Corey Davis, Ph.D. LifeSci Advisors Phone: +1 212 915 2577 Email: cdavis@lifesciadvisors.com

 

AI algorithm detects signs of Alzheimer's disease through language

You will want your doctor to test you with this to create a baseline for you and have you use the dementia prevention protocols you doctor should have available.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

The latest here:

AI algorithm detects signs of Alzheimer's disease through language 

 

With no cure and no straightforward way of diagnosing the disease, scientists are exploring every avenue when it comes to detecting Alzheimer’s during its early stages. One group of researchers has turned its attention to subtle differences in the language of sufferers, and have developed an AI tool they say can pick up on these as a way of potentially screening for the disease.

The research was carried out at New Jersey's Stevens Institute of Technology and focuses on the way some Alzheimer’s sufferers express themselves. The disease, and others that cause dementia, can impact some parts of the brain that control language, meaning that sufferers can struggle to find the right words, perhaps using the word “book” to describe a newspaper, or replacing nouns with pronouns, for example.

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“Language deficits occur in eight to 10 percent of individuals in the early stages of Alzheimer’s disease (AD), and become more severe and numerous during its later stages,” lead author of the study, K.P. Subbalakshmi explains to New Atlas. “Note that this statistic is only valid for the early stages of AD. That said, it is standard practice in clinical settings to use language as a way to screen for AD.”

Subbalakshmi and her students set out to develop an AI tool that could detect these language differences, by turning to a standard picture description task currently used in language screening for Alzheimer’s. This asks subjects to describe a drawing of children stealing cookies from a jar, and the team drew on existing transcripts of more than 1,000 interviews, from both Alzheimer’s patients and healthy controls.

These texts were used to train the AI algorithm, with the individual sentences broken down and assigned numerical values so the system could analyze the structural and thematic relationships between them. Over time, this enabled the algorithm to learn to distinguish between the sentences spoken by healthy subjects and Alzheimer’s sufferers with more than 95-percent accuracy, according to the team. Furthermore, it can also explain why it came to the conclusions that it did.

“This is a real breakthrough,” says Subbalakshmi. “We’re opening an exciting new field of research, and making it far easier to explain to patients why the AI came to the conclusion that it did, while diagnosing patients. This addresses the important question of trustability of AI systems in the medical field.”

From here, the team hopes to expand the tool for use in languages other than English, and even enable it to diagnose Alzheimer’s using other types of text, such as an email or social media post. The researchers also see great potential in using it to track how the disease progresses over time, as a way of detecting it in its very early stages.

“We are exploring other angles of interpretability of the AI and also looking to find datasets that has a time evolution factor to it,” explains Subbalakshmi. “That is, a dataset that tracks patient's language abilities as time progresses. This will help us develop personalized detection for individuals that are at risk of developing this disease.”

The researchers presented their research at last month’s 19th International Workshop on Data Mining in Bioinformatics.

Source: Stevens Institute of Technology

Researchers discover quirk of cell aging that could help detect late-onset Alzheimer's

You likely need this so you can kick your dementia prevention into high gear. NO research will occur because of this since we have NO stroke leadership working on solving all the problems in stroke. You're screwed.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

 Researchers discover quirk of cell aging that could help detect late-onset Alzheimer's

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October 30, 2017

Researchers at The University of Texas Health Science Center at Houston (UTHealth) School of Dentistry and McGovern Medical School have discovered a previously unknown characteristic of brain-cell aging that could help detect late-onset Alzheimer's disease decades before symptoms begin.
The study, "Interleukin33 deficiency causes tau abnormality and neurodegeneration with Alzheimer-like symptoms in aged mice," appeared online in the journal Translational Psychiatry earlier this year.
Working with mice, the UTHealth team found that neurons in the brain experienced a sudden increase in aging around the mouse equivalent of age 40 in humans. Normal mice responded with a surge of interleukin33, a protein that activates the body's repair mechanisms to make the neurons healthy again. Mice lacking the IL33 gene didn't experience the surge and continued to decline, eventually developing dementia at an age roughly equivalent to 68 in humans.
"We think we're getting old gradually, but when we're talking about these cells, we've discovered that it's not that way," said Yahuan Lou, Ph.D., a professor in the Department of Diagnostic and Biomedical Sciences at the School of Dentistry.
Late-onset sporadic Alzheimer's disease occurs after age 65 and represents approximately 95 percent of all cases, with the other 5 percent believed to be genetic. By the time symptoms appear, the brain has already lost massive numbers of neurons. The UTHealth researchers believe the surge at age 40 may be an ideal time to look for biomarkers that predict Alzheimer's long before the damage begins.
Lou first detected the power of IL33 while studying premature ovarian failure in mice. "We observed that when we removed IL33, the ovary shrank much faster than normal. So we wondered: If IL33 does this in the ovary, what does it do in the brain? The brain has an abundance of IL33."
Looking for collaborators who could test that question, Lou was surprised to learn that researchers from McGovern Medical School's Department of Psychiatry and Behavioral Sciences had recently moved into the new UT Behavioral and Biomedical Sciences Building that he and other dental school researchers had also newly occupied. Among his new neighbors were Department of Psychiatry Professor Joao De Quevedo, M.D., Ph.D., and Assistant Professor Ines Moreno-Gonzalez, Ph.D., of the Mitchell Center for Alzheimer's Disease, who had the expertise and resources for analyzing rodent behavior and correlating it to humans. A collaborative team soon formed, and their mouse study led to the paper in Translational Psychiatry with plans for follow-up studies to explore the tantalizing results.

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Lou said a group of researchers in Singapore recently conducted an experiment using mice that model familial early-onset Alzheimer's disease. "When they injected IL33 into the [Alzheimer's] mice, they saw that the plaque load was reduced, but they didn't know why," he said. "We've figured out why."
The IL33 injections seemed to relieve symptoms temporarily, he added, but did not cure the disease. The effects lasted about two weeks in mice -- equal to several months in humans. Lou believes finding a way to enhance the brain's own supply of IL33 may lead to potential treatments for the disease.
The cause of late-onset Alzheimer's is a medical mystery with many potential causes under investigation, including neuro-inflammation, abnormal aging, smoking, and infections. IL33 deficiency is another promising lead, with additional studies planned as funding is secured.

Source:

https://dentistry.uth.edu/about/news-media/story.htm?id=805e57d5-01a2-4353-8a46-86424e661b9a

Undergraduates earn top prize for developing new tool to detect Alzheimer’s disease

A great stroke association would immediately hire all of them and set them to work solving all the problems in stroke, but since we have fucking failures of stroke associations this possibility will slip through their fingers. And you as a stroke survivor will likely not recover much more and your children and grandchildren will be screwed if they have a stroke. 
https://www.news-medical.net/news/20170829/Undergraduates-earn-top-prizec2a0for-developing-new-tool-to-detect-Alzheimere28099s-disease.aspx

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August 29, 2017

A team of seven University of Maryland A. James Clark School of Engineering undergraduates earned the top prize in this year's National Institutes of Health (NIH) Design by Biomedical Undergraduate Teams (DEBUT) challenge for their efforts to develop low-cost tools to diagnose Alzheimer's disease before patients show symptoms.
"This represents a monumental achievement, not simply for the engineering community, but for the wider world of human health research," said Darryll J. Pines, dean of the Clark School and Nariman Farvardin Professor. "As rising sophomores, these seven students in many ways represent the future of biomedical innovation. Through collaborations with faculty and researchers across a range of disciplines, they have transformed ideas into innovation that could one day change how Alzheimer's and other diseases are diagnosed."
The team, known as "Synapto," was awarded $20,000 from the NIH National Institute of Biomedical Imaging and Bioengineering (NIBIB) for developing a portable electroencephalogram (EEG) that uses a specially designed headset and a new software analysis tool to detect Alzheimer's disease before a patient displays clinical symptoms. The device exploits changes observed in the brainwaves of Alzheimer's patients in response to special auditory tones. The team, which recently filed for a company LLC in Maryland, believes their work could help make dementia diagnosis more quantitative, more systematic, and less costly - allowing doctors to use it at regular check-ups.
"Alzheimer's disease is the sixth leading cause of death in the United States, costing the nation close to $259 billion this year," said UMD Fischell Department of Bioengineering (BIOE) undergraduate and Synapto team captain Dhruv Patel, citing data from the Alzheimer's Association. "Diagnosing the disease early on allows patients to open up treatment options, manage the disease properly, and slow its progression."
Today, PET scans, MRIs, and spinal taps are most commonly used to diagnose Alzheimer's disease. Such methods are expensive and, at times, invasive, so many patients are diagnosed based only on their symptoms.
"It can take up to two years after clinical symptoms arise for patients to receive a proper diagnosis, and by then, he or she may have already seen significant progression of the disease," Patel said. "To address this, our technique allows us to characterize an Alzheimer's patient's brainwave using a variety of mathematical analytical tools and compare it with a healthy patient's brainwave to create a machine-learning model that can then accurately predict the probability of the patient having the disease."

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"Synapto's project serves as a prime example of how tomorrow's bioengineers are working today to find solutions to some of the most significant health challenges our society faces," said John Fisher, Fischell Family Distinguished Professor and BIOE chair. "It is inspiring to see our students driven to make a real-world impact so early in their academic careers, and I look forward to their future successes."
Organized by the UMD student chapter of the Biomedical Engineering Society (BMES-UMD), Synapto's team members are: BIOE students David Boegner, Megha Guggari, Chris Look (a computer science double-major), Anoop Patel, and Dhruv Patel; and Department of Chemical and Biomolecular Engineering students Megan Forte and Brianna Sheard, a recent transfer from UMD. The group's participation in the competition was led, in part, by the BMES-UMD executive board and supported by faculty advisor Steven Jay, a BIOE assistant professor. Bill Idsardi, chair of UMD's Department of Linguistics, provided the initial hardware that helped accelerate the project.
The DEBUT challenge this year awarded $65,000 in prizes, supported by a public-private partnership between NIBIB and VentureWell, a non-profit higher-education network that cultivates revolutionary ideas and promising inventions. Of 41 eligible entries received from 22 universities across 16 states, NIBIB selected three winning teams based on the significance of the problem addressed, impact on clinical care, innovation of design, and evidence of a working prototype. VentureWell selected two additional teams based on market potential and patentability.

Source:

http://eng.umd.edu/release/bioe-chbe-undergraduates-develop-tools-to-diagnose-alzheimers-disease-before-patients-show-symptoms

The RUDAS Dementia Test is brief, effective and free. It works well for most people.

Don't do this on your own, it requires a trained interpreter.  You will need this, but I bet your doctor does no baseline testing,

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

 

The RUDAS Dementia Test is brief, effective and free. It works well for most people.

A key study reports that the Rowland Universal Dementia Assessment Scale (RUDAS) is an effective dementia test. The study shows this is particularly true in multicultural populations, where English is not a patient's first language.

The study was published in CMAJ (Canadian Medical Association Journal).

The Results

Popular tests used by doctors to assess cognitive health include the MMSE (Mini-Mental State Examination) and the MCA (Montreal Cognitive Assessment). Though widely used, they can be difficult and overly-challenging for patients with low education levels, as well as those whose first language is not English.

Researchers undertook a systematic review and meta-analysis to determine whether the RUDAS, developed in Australia in 2004, is effective in a variety of settings. They also wanted to understand how it compares to other tests. The study included 1236 people from 11 previous studies conducted in 6 countries. The mean age of participants was 73.5 years, and almost two-thirds (61%) were female.

The results showed that RUDAS was consistently free of cultural and educational bias in multicultural samples.

What It Looks Like

The RUDAS includes questions such as recall of four grocery items, what safety precautions should one take when crossing the street, and naming of animals in 1 minute; it also assesses coordinated movements.

The test appeared to be effective in identifying cognitive impairment and ruling it out across various cultures because language and education had less effect on results than with the other assessment tools.

Limitations

Other Popular Tests

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SAGE Pen & Paper Alzheimer's Test

VIDEO+ARTICLE:

Problems with memory or thinking? Check out this simple, written exam from Ohio State University Medical Center. Find out what made this outstanding test go viral.

Read more »

The authors noted that all studies included in the analysis used trained interpreters; this may be a limitation since interpreters will not always be available for tests in all settings.

RUDAS is easily interpreted by an interpreter during an assessment. Some translated versions are available but are not validated.

Conclusions

"Given our aging immigrant population... and the anticipated increase in dementia prevalence worldwide in coming decades, earlier and more accurate detection of dementia in these populations will become increasingly important," writes Dr. Raza Naqvi, a geriatrician with the Schulich School of Medicine & Dentistry, Western University, London, Ontario, Canada, with coauthors.

"The RUDAS is a freely available, effective brief cognitive assessment tool that has shown strong psychometric properties in several countries. It shows particular advantage in culturally and linguistically diverse populations," the authors conclude.

The Test:

1. Listen to an interview with the author (Podcast): https://soundcloud.com/cmajpodcasts/naqvi-multicultural-cognitive 
2. Video on how to administer and score the RUDAS test:. (Running time: 20 minutes) Online RUDAS Video 
3. RUDAS administration and scoring guide - English (PDF: 25 page booklet) 
4. RUDAS scoring sheet - English (PDF) 
5. RUDAS scoring sheet - Chinese (PDF) 
6. RUDAS scoring sheet - Italian (2 pages looseleaf) 

Continued below ad...

MORE INFORMATION:

• Cognitive assessments in multicultural populations using the Rowland Universal Dementia Assessment Scale: a systematic review and meta-analysis , Raza M. Naqvi, Sehrish Haider, George Tomlinson, Shabbir Alibhai. CMAJ, DOI:10.1503/cmaj.140802.

SOURCE:

• CMAJ (Canadian Medical Association Journal)

Non-Invasive Eye Scan Could Detect Signs of Alzheimer’s Years Before Patients Show Symptoms

After your doctor runs this test, what are the EXACT effective dementia prevention protocols you are prescribed?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Non-Invasive Eye Scan Could Detect Signs of Alzheimer’s Years Before Patients Show Symptoms 

August 18, 2017

LOS ANGELES -- August 18, 2017 -- Alzheimer’s disease affects the retina similarly to the way it affects the brain, according to a study published in JCI Insight.
The study also revealed that an investigational, non-invasive eye scan could detect the key signs of Alzheimer’s disease years before patients experience symptoms.
Using a high-definition eye scan developed especially for the study, researchers detected the crucial warning signs of Alzheimer’s disease: amyloid-beta deposits. The findings represent a major advancement toward identifying people at high risk for the debilitating condition years sooner.
“The findings suggest that the retina may serve as a reliable source for Alzheimer’s disease diagnosis,” said Maya Koronyo-Hamaoui, PhD, Cedars-Sinai Medical Center, Los Angeles, California. “One of the major advantages of analysing the retina is the repeatability, which allows us to monitor patients and potentially the progression of their disease.”
Another key finding from the study was the discovery of amyloid plaques in previously overlooked peripheral regions of the retina. The researchers found that the amount of plaque in the retina correlated with plaque amount in specific areas of the brain.
“Now we know exactly where to look to find the signs of Alzheimer’s disease as early as possible,” said Yosef Koronyo, Cedars-Sinai Medical Center.
“Our hope is that eventually the investigational eye scan will be used as a screening device to detect the disease early enough to intervene and change the course of the disorder with medications and lifestyle changes,” said Keith L. Black, MD, Cedars-Sinai Medical Center.
The study included 16 patients with Alzheimer’s disease. The patients drank a solution that included curcumin, which causes amyloid plaque in the retina to light up and be detected by a modified scanning laser ophthalmoscope. The patients were then compared to a group of 37 younger, cognitively normal individuals.
Histological examination uncovered classical and neuritic-like Abeta deposits with increased retinal amyloid-beta 42 plaques (4.7-fold; P = .0063) and neuronal loss (P = .0023) in patients with AD versus matched controls. Retinal amyloid-beta plaque mirrored brain pathology, especially in the primary visual cortex.
Reference: https://doi.org/10.1172/jci.insight.93621
SOURCE: Cedars-Sinai Medical Center

Brain scanning could improve dementia diagnosis for two thirds of patients, study finds

You'll likely need this so ask your doctor for a baseline while you can still remember.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Brain scanning could improve dementia diagnosis for two thirds of patients, study finds

Sarah Knapton

,

The Telegraph•July 16, 2017

Routine brain scanning could improve dementia diagnosis for two thirds of patients, ending years of misdiagnosis, a study has found. 

Currently the only way to determine whether Alzheimer’s is present is to look at the brain of a patient after death.

For patients who are still alive, doctors usually use special cognitive tests which monitor memory and everyday skills such as washing and dressing, but the results are often be misleading or inaccurate. 

Now new findings presented at the Alzheimer’s Association International Conference in London show that Positron Emission Tomography (PET) scans altered the diagnoses for more than two thirds people.

Currently people with early stage Alzheimer’s can wait up to four years to receive a correct diagnosis because PET scans are rarely carried out on the NHS as they cost up to £3,000 a time.

But PET scans show the build-up of sticky amyloid plaques in the brain which prevent neurons from communicating and eventually kill areas, wiping out memories and can help with a definitive diagnosis.

Thousands of people are misdiagnosed because the NHS does not carry out routine brain scanning for people with suspected dementia  Credit: Paula Solloway/Alamy 

Not only do scans pick up problems early, when drugs or lifestyle changes could make a difference, but they could also help reassure people who are suffering mild memory problems that they do not have the disease.

Dr David Reynolds, Chief Scientific Officer at Alzheimer’s Research UK said: “Diagnosing dementia is a complex challenge, and doctors have to gather a range of clues to create a picture of what is going on in the brain.

“This new research highlights that value that amyloid brain scans can bring in helping doctors make a more informed diagnosis, either by indicating or ruling out Alzheimer’s as the possible cause of someone’s dementia symptoms.

“The current drive for life-changing dementia treatments means that in the future, the use of amyloid PET scans or other innovative diagnostic methods will be important to ensure that new medicines reach the right people at the right time.”

Positron Emission Tomography (PET) scans work by picking up how good parts of the brain are at sucking up glucose, which is injected into the body bound to a radioactive tracer which can be seen on screen. Parts of the brain that are clogged up and not functioning will not light up. 

The new study by the Karolinska Institute in Sweden involving 135 people who had been referred for memory problems found that 68 per cent had a change in diagnosis, following the scans.

A separate study led by GE Healthcare in the UK analysed data from four previous studies looking at the use of brain amyloid PET scans in the process of dementia diagnosis, combining information from 1106 people, found the use of brain amyloid PET scans led to a change in diagnosis in 20 per cent of people.

“A negative brain PET scan indicating sparse to no amyloid plaques rules out Alzheimer’s disease as the cause of dementia symptoms,” said Dr James Hendrix, Alzheimer’s Association Director of Global Science Initiatives.

“This makes it a valuable tool to clarify an uncertain or difficult diagnosis. Misdiagnosis is costly to health systems, and expensive and distressing to persons with dementia and their families.”

This 5-minute test could detect if you are at risk for Alzheimer's disease

I could find no research in Google Scholar so I have no clue what proof this has that it works.
But this is on their website;
Our Imprint Check-Up is based on a landmark research study by Dr. Stuart Zola at Emory University. Dr. Zola found that participants’ performance on a longer 30-minute assessment was highly predictive of their cognitive decline. He tracked each person's level of cognitive decline and then correlated it with his or her assessment result over 3 years.
The president discussing it here; 2:13 video;
https://www.youtube.com/watch?v=YOn2TzvZS1U
The basic website for the marketing push here:
https://www.neurotrack.com/
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Your doctor should be following this up so you have a baseline measurement before you get dementia/Alzheimers.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.
If you have anything close to a decent doctor a protocol will already be in place to prevent this from occurring.  

Diet and exercise can reduce protein build-ups linked to Alzheimer’s, UCLA study shows

I'm positive your doctor and hospital will not follow this up by creating diet stroke protocols for you. You are completely on your own. Guess wrong and you might get Alzheimers and your doctor will never acknowledge their complicity in you getting Alzheimers.
http://www.mdlinx.com/neurology/top-medical-news/article/2016/08/17/13

UCLA Health System

A study by researchers at UCLA’s Semel Institute for Neuroscience and Human Behavior has found that a healthy diet, regular physical activity and a normal body mass index can reduce the incidence of protein build–ups that are associated with the onset of Alzheimer’s disease. In the study, 44 adults ranging in age from 40 to 85 (mean age: 62.6) with mild memory changes but no dementia underwent an experimental type of PET scan to measure the level of plaque and tangles in the brain. Researchers also collected information on participants’ body mass index, levels of physical activity, diet and other lifestyle factors. Plaque, deposits of a toxic protein called beta–amyloid in the spaces between nerve cells in the brain; and tangles, knotted threads of the tau protein found within brain cells, are considered the key indicators of Alzheimer’s. The study found that each one of several lifestyle factors — a healthy body mass index, physical activity and a Mediterranean diet — were linked to lower levels of plaques and tangles on the brain scans. “The fact that we could detect this influence of lifestyle at a molecular level before the beginning of serious memory problems surprised us,” said Dr. David Merrill, the lead author of the study, which appeared in the September issue of the American Journal of Geriatric Psychiatry.

Imaging technology allows 3-D visualization of Alzheimer’s-related plaques

Your doctor should be following this up so you have a baseline measurement before you get dementia/Alzheimers.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.
If you have anything close to a decent doctor a protocol will already be in place to prevent this from occurring.   
 
http://medcitynews.com/2016/07/imaging-visualization-alzheimer/?utm_source=hs_email&utm_medium=email&utm_content=31759017&_hsenc=p2ANqtz-9xRPeh25C-cuRq1WVy5tXJWE84eeVzTZXtOVLYArknaDLUeLJd1wdF44JRsmGuBun4dJuY_5ixWY1ujIdL5TvonMojIw&_hsmi=31759017
A nonprofit dedicated to finding a cure for Alzheimer’s disease is funding a new technology that allows greater visualization of amyloid plaques as well as other Alzheimer’s markers, such as tau proteins and vasculature and microglia activation.
The technology was created by scientists at the New York City-based Fisher Center for Alzheimer’s Research Foundation and described in a study published in the scientific journal Cell Reports. Dr. Marc Flajolet, lead author of the study and team leader, said the new technology platform allows the visualization of those markers in larger, three-dimensional amyloid patterns (TAPs) in greater volume. Fisher Center scientists conducted their research on brain tissue from mice and frozen human brain samples of deceased Alzheimer’s patients.
“We are proud that the funding we provide has resulted in innovative, never- before-seen imaging of what causes Alzheimer’s disease,” said Kent Karosen, Fischer Center president and CEO. “The Fisher Center scientists are working diligently to better understand the cause and cure of the disease and with the ability to visualize the causes of Alzheimer’s, we’re one step closer to a cure.”
Flajolet said the Fisher’s team employed the “iDISCO” visualization method involving targeted molecular labeling, tissue clearing and light-sheet microscopy.
The new technology allows 3-D visualization in five different brain regions, better mapping and automated detection enabling faster quantification of plaques, which Flajolet characterized as a cheaper alternative to standard beta amyloid plaque labeling.
“Now we can look at much bigger volumes and see bigger structures that we could not see before in higher resolution,” he explained. “Before this, there were more limitations. We were unable to get the detail we get now.”
He said the technology may open doors of possibility for further Alzheimer’s research that might lead to new Alzheimer’s disease classifications.
“What we have discovered is that amyloid plaques (the groupings of protein that mark the presence of Alzheimer’s) organize themselves into strange patterns that are distributed in different ways, in some cases layers of plaques,” he said. “We don’t yet understand the meaning. But if we could organize patients by how those plaques presented themselves in the brain through retrospective studies and learn the symptoms those patients expressed, we might find ways to categorize stages of the disease differently.”
He said that today, new drugs are tested on Alzheimer’s patients without regard to the level or patterns of plaque in their brains.
“But perhaps, like depression or schizophrenia, not all patients respond to the same drugs. Could it be the same for Alzheimer’s?” Flajolet wondered. “If we are dealing with brains and we know patient symptoms, there is a chance we could propose some categories so the next clinical trial might be used on different patients expressing different patterns. It might only work on 10 percent of patients, but it could open doors.”
The Fisher Center for Alzheimer’s Research Foundation was established in 1995 by philanthropists Zachary Fisher and David Rockefeller. Paul Greengard, who leads the research center, is a Nobel Prize-winning scientist, leads a team of 50 researchers seeking a cure for Alzheimer’s.
Here’s a video from the Fisher Center demonstrating the visualization:

Metallic molecule offers real-time monitoring of amyloid plaques in patients with Alzheimer's

Your doctor should be following this up so you have a baseline measurement before you get dementia/Alzheimers.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.
If you have anything close to a decent doctor a protocol will already be in place to prevent this from occurring.   

http://www.news-medical.net/news/20160711/Metallic-molecule-offers-real-time-monitoring-of-amyloid-plaques-in-patients-with-Alzheimers.aspx

A metallic molecule being studied at Rice University begins to glow when bound to amyloid protein fibrils of the sort implicated in Alzheimer's disease. When triggered with ultraviolet light, the molecule glows much brighter, which enables real-time monitoring of amyloid fibrils as they aggregate in lab experiments.
Rice chemist Angel Martí said such a powerful probe could be a boon to researchers seeking a way to break up amyloid plaques, which form in the brains of patients with Alzheimer's. Martí's lab reported on the light-switching molecule in the Journal of the American Chemical Society. Rice graduate student Amir Aliyan is lead author of the paper.
Martí and his team study dyes made of metallic complexes that luminesce when attached to amyloid fibrils or DNA. They discovered that when rhenium dipyridophenazine complexes bind with an amyloid fibril in a test tube and are excited with ultraviolet light, the synthetic molecules increase their natural photoluminescence by several orders of magnitude.
"Most dyes decrease their fluorescence upon continuous excitation because they photobleach," Martí said. "This dye does the complete opposite, increasing its emission even more every time you excite it." The effect isn't nearly as strong if the metallic molecule is either floating in a solution or attached to single amyloid strands, he said.
The effect is seen in two stages, he said. The probe incorporates a hydrophobic part that naturally binds to aggregating fibrils and emits light when it does, giving researchers a clear signal that aggregation is happening. Exciting the combined aggregate and probe with ultraviolet light then boosts the light output more than a hundredfold.
The Rice researchers suspect the dramatic increase happens when reactive oxygen species attack the amino acids on the amyloid beta fibril that would normally quench the luminescence of the metal complex.
"Our hypothesis is that upon ultraviolet irradiation, our (rhenium) metal complex produces reactive oxygen species and they're more aggressive than conventional molecular oxygen," Aliyan said. "There are reports that rhenium complexes are capable of activating oxygen from one form to a more aggressive form in solution."

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"That's one of our theories," Martí added. "We still don't understand well what is happening. But we know that besides increasing the emission intensity, the complex also chemically modifies the (amyloid) protein."
Martí said experiments that removed as much oxygen as possible eliminated the enhanced fluorescence effect. He said the lab stepped back to test an earlier metallic complex based on ruthenium, which also showed emission when attached to amyloid fibrils. It did not show enhanced emission under ultraviolet light.
"We thought the effect might be happening with ruthenium and we had completely missed it, so we ran a control experiment and nothing happened," he said.
That makes the rhenium complex unique so far. It also gives researchers the opportunity to learn more about amyloid beta proteins and the mechanics of aggregation, Martí said.
"We've always been interested in knowing where these complexes bind," he said. "If they oxidize amyloid beta in the periphery of their binding site, then by tracking the place of oxidation we will know the place of binding. That is called footprinting. It will allow us to specifically explore binding and how chemical modification of the surface of the protein would affect factors like toxicity and aggregation."
Aliyan said the probe allows real-time protein aggregation study as the probe turns on upon aggregation. "To the naked eye, aggregation is not obvious," he said. "You need a probe to follow the process and see if potential drugs can inhibit aggregation or make it faster or slower. Then you can run assays with or without any drug and in a variety of conditions. One would think if there are ways to modify amyloid beta aggregation, maybe there are ways to treat the process."

Source:

Rice University

Scientists create new eye technology for detecting Alzheimer's before onset of symptoms

Your doctor should be following this up so you have a baseline measurement before you get dementia/Alzheimers.
1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.
If you have anything close to a decent doctor a protocol will already be in place to prevent this from occurring. 

http://www.news-medical.net/news/20160711/Scientistsc2a0create-new-eye-technology-for-detecting-Alzheimers-before-onset-of-symptoms.aspx

Scientists may have overcome a major roadblock in the development of Alzheimer's therapies by creating a new technology to observe - in the back of the eye - progression of the disease before the onset of symptoms. Clinical trials are to start in July to test the technology in humans according to a paper recently published in Investigative Ophthalmology & Visual Science (IOVS).
The paper, titled Early detection of amyloidopathy in Alzheimer's mice by hyperspectral endoscopy, builds upon previous work in cells by detecting changes in the retina of mice predisposed to develop Alzheimer's.
Early detection of Alzheimer's is critical for two reasons. "First, effective treatments need to be administered well before patients show actual neurological signs," said author Robert Vince, PhD, of the Center for Drug Design at the University of Minnesota (UMN). "Second, since there are no available early detection techniques, drugs currently cannot be tested to determine if they are effective against early Alzheimer's disease. An early diagnostic tool like ours could help the development of drugs as well."
Looking through the eye to see the brain is a key advantage of the new technology. "The retina of the eye is not just 'connected' to the brain — it is part of the central nervous system," said author Swati More, PhD, also of the Center for Drug Design at UMN. While the brain and retina undergo similar changes due to Alzheimer's disease, "unlike the brain, the retina is easily accessible to us, making changes in the retina easier to observe."
"We saw changes in the retinas of Alzheimer's mice before the typical age at which neurological signs are observed," said More. "The results are close to our best-case scenario for outcomes of this project."

Source:

Association for Research in Vision and Ophthalmology (ARVO)