Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label p-tau181. Show all posts
Showing posts with label p-tau181. Show all posts

Monday, July 20, 2026

New study suggests unexpected link between long sleep and Alzheimer’s

 But do you have cause and effect correct? Early undetected Alzheimers may cause long sleep!

New study suggests unexpected link between long sleep and Alzheimer’s

Researchers found that older adults who routinely sleep 10 hours or more a night had elevated levels of a blood protein considered an early warning sign of dementia.

Sleeping long hours every night may be linked to elevated levels of a blood protein widely regarded as a telltale sign of Alzheimer’s disease, according to a new study by the University of Texas at San Antonio’s academic health center.

UT Health San Antonio reports that, among the 2,410 participants, those who slept 8.5 to nine hours a night had higher levels of phosphorylated tau 181, or p-tau181, a modified form of tau protein associated with cognitive decline. Researchers said p-tau181 levels increased “most sharply” among sleepers who slept more than 10 hours a night. “A lot of people worry about whether their sleep habits are affecting their brain health,” said Vanessa M. Young, PhD, MS, a postdoctoral research fellow at the center’s Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases. “Because this is a snapshot in time rather than a long-term study, we cannot say that long sleep causes Alzheimer’s, but the findings suggest it may be worth monitoring, and that more sleep is not always better for brain health.”

Participants had an average age of 70. Just over 55 percent were female.

Related video: Alzheimer's disease study (KARE-TV Minneapolis St. Paul)The study follows up onby UT Health San Antonio that found sleeping nine or more hours a night was associated with worse cognitive performance, especially among people diagnosed with depression. The latest study, conducted by some of the same researchers, was more extensive. It accounted for multiple health factors and examined blood-based markers that have been tied to Alzheimer’s and neurodegeneration in relation to participants’ self-reported sleep hours. “Sleep is a promising modifiable risk factor linked to the disease,” researchers said, “but existing evidence has remained limited and inconclusive.” people diagnosed with depression. The latest study, conducted by some of the same researchers, was more extensive. It accounted for multiple health factors and examined blood-based markers that have been tied to Alzheimer’s and neurodegeneration in relation to participants’ self-reported sleep hours. “Sleep is a promising modifiable risk factor linked to the disease,” researchers said, “but existing evidence has remained limited and inconclusive.”

Three other proteins associated with brain cell damage were also tested but, unlike p-tau181, they appeared to have no association with sleep duration, researchers said.

While the study found elevated levels of p-tau181 among habitual long sleepers, UT Health San Antonio said more research is needed to determine whether the association can ultimately be tied to Alzheimer’s risk.

The center’s findings coincide with a study published last week in JAMA that said simple blood tests may be able to predict who will develop cognitive impairment up to a decade before the first symptoms surface. The most accurate test measured levels of a mutation of a different tau protein, phosphorylated tau 217 (p-tau217).

The study of nearly 2,700 older adults on three continents found that people with high levels of the p-tau217 biomarker had a 38 percent chance of developing cognitive impairment within five years and a 78 percent chance within 10 years.

Further research and clinical trials could lead to the development of new therapies that may one day slow or even stop Alzheimer’s progression, researchers said.

An estimated 57 million people worldwide are affected by dementia, the San Antonio study noted, with Alzheimer’s diagnosed in 60 to 70 percent of all cases.

“Even with recent advances in disease-modifying therapies, Alzheimer’s remains a profound medical and societal challenge,” researchers said.

Young suggested that long sleepers might want to bring up the new study’s findings during their next doctor visit. “In plain terms, if you regularly find yourself sleeping nine to 10 hours or more a night,” she said, “it may be worth mentioning to your doctor as a useful conversation starter about your sleep quality and overall brain health.”

This post originally appeared at inc.com.

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Tuesday, August 19, 2025

Heart Drug From Nearly-Forgotten Class May Treat Alzheimer's

 Incomplete research, nothing here tells us if treatment prevents Alzheimers, so completely fucking useless. Biomarkers do nothing towards recovery!

Heart Drug From Nearly-Forgotten Class May Treat Alzheimer's

Biomarker effects strongest in APOE4 carriers

by , Contributing Writer, MedPage Today

TORONTO -- Biomarkers pointing to increased risk for Alzheimer's disease were markedly reduced with the investigational cholesteryl ester transfer protein (CETP) inhibitor obicetrapib relative to placebo in a large phase III trial, a researcher reported here.

Median levels of phosphorylated tau protein-217 (p-tau217), a key Alzheimer's biomarker, rose 2.5-fold faster with placebo than with obicetrapib over 12 months, according to Philip Scheltens, MD, PhD, of VU Medical Center in Amsterdam, speaking at the Alzheimer's Association International Conferenceopens in a new tab or window.

Other biomarkers such as p-tau181 and the ratio of amyloid beta-42 to its 40-residue form (Aβ42/40) also indicated a potential(Research should give us actual and your mentors didn't request that? Bad research!) risk reduction with the drug among more than 1,500 individuals with cardiovascular disease.

This was from a prespecified secondary analysis of data from a cardiovascular-focused trial of obicetrapib called BROADWAY, primary results from which were reported in Mayopens in a new tab or window. The drug works by blocking conversion of high-density lipoprotein (HDL) cholesterol into the low-density form (LDL). CETP inhibitors were all the rage a few years ago as a novel approach to cholesterol management, but poor results with the first wave of candidates didn't meet expectationsopens in a new tab or window. But obicetrapib's developer, Netherlands-based NewAmsterdam Pharma, didn't give up. BROADWAY is one of three phase III trials to examine the drug's safety and efficacy in reducing LDL levels; another trial is underwayopens in a new tab or window that will show whether it also reduces major cardiovascular events.

But research on the interplay of cholesterol metabolism and Alzheimer's disease led the company to keep an eye on obicetrapib's effects on Alzheimer's disease biomarkers. "Lipid dysregulation is very important for Alzheimer's disease, it's an important risk factor, especially with APOE4," he told attendees. "Obicetrapib actually has the ability to significantly change p-tau progression over time as compared with placebo."

BROADWAY had a total of 2,530 participants with either familial hypercholesterolemia or established atherosclerotic cardiovascular disease, randomized 2:1 to obicetrapib or placebo for 12 months. Scheltens's presentation focused on 1,515 participants who were designated for Alzheimer's biomarker analyses. Of these, 367 carried at least one copy of the APOE4 gene. Trajectories for p-tau217 and the Aβ42/40 ratio were the primary outcomes.

Patients in the active drug group showed a 1.99% increase in p-tau217 over the year of treatment, compared with 4.98% with placebo (P=0.019); no significant difference in the Aβ42/40 trajectory was seen (-0.44% vs 1.03%, P=0.29).

But an exploratory endpoint, the ratio of p-tau217 to Aβ42/40, did show a very significant difference, with increases of 2.51% with obicetrapib compared with 6.55% in the placebo group (P=0.004).

Differences between groups were also greater in APOE4 carriers. In the latter, p-tau217 increased 1.45% with the drug versus 7.19% with placebo (P=0.022); this pattern was also seen for older APOE4 carriers. The gap grew even larger when Scheltens and colleagues looked at the 29 homozygous APOE4 carriers: a decrease of 7.81% with obicetrapib, compared with a 12.67% spike in the placebo group.

The investigators' belief, Scheltens said, is that these effects are not a consequence of diminished HDL-LDL conversion, but rather some type of direct action on Alzheimer's pathology.

He also noted that safety findings were highly favorable, with no differences from placebo in the BROADWAY sample.

NewAmsterdam has not revealed specific plans for pursuing obicetrapib as an Alzheimer's therapy, concentrating for now in securing approval for cardiovascular indications.

Thursday, June 5, 2025

The Role of Phosphorylated-Tau 181 in Enhancing Neuroplasticity After Ischemic Stroke

Interesting, good for stroke recovery, bad for Alzheimer's. Your competent? doctor will need to ensure your levels are correct at each point in your stroke recovery. I bet your incompetent? doctor can't do that!

 The Role of Phosphorylated-Tau 181 in Enhancing Neuroplasticity After Ischemic Stroke


Lasta Arshinta, Ketut Widyastuti*, I Putu Eka Widyadharma
Neurology Department, Faculty of Medicine, Universitas Udayana,
Ngoerah General Hospital, Denpasar, Indonesia
*Corresponding author details: Ketut Widyastuti; kt_widyastuti@unud.ac.id
ABSTRACT
Ischemic stroke is a predominant cause of neurological impairment globally. Notwithstanding progress in acute treatment, the long-term functional recovery of individuals continues to be constrained. Recent research has concentrated on the function of neurodegenerative biomarkers, particularly phosphorylated tau 181 (p-tau 181), in influencing neuroplasticity following ischemic stroke. This study seeks to investigate the function of p-tau 181 in augmenting neuroplasticity following ischemic stroke. This investigation was performed by literature analysis and examination of experimental data from animal models and human subjects. The findings indicated that p-tau 181 levels were markedly elevated during the subacute phase post-stroke and correlated with the reconfiguration of brain circuits facilitating the recovery of motor and cognitive functioning. The mechanisms involved encompass enhanced synaptic connection, the induction of neurogenesis, and augmented myelination. While p-tau 181 is frequently linked to the neurodegenerative mechanisms of Alzheimer's disease, in the setting of stroke, the transient elevation of p-tau 181 seems to serve an adaptive function to facilitate recovery. These findings create new prospects for the advancement of biomarker-driven therapy techniques to enhance post-stroke recovery. Nonetheless, additional investigation is required to comprehend the physiological and pathological thresholds of p-tau 181 and its possible long-term implications.
Keywords: phosphorylated-tau 181; neuroplasticity; ischemic stroke.

Monday, January 13, 2025

Brain Connectivity Patterns Link Vascular Disease to Cognitive Decline

 How will your competent? doctor EXACTLY PREVENT THIS POST STROKE? NO plan? So, you don't have a functioning stroke doctor, do you?

Brain Connectivity Patterns Link Vascular Disease to Cognitive Decline

Summary: Researchers have identified how cerebrovascular disease (CeVD) disrupts brain connectivity, contributing to cognitive decline and neurodegeneration alongside Alzheimer’s disease (AD). By studying brain networks and blood biomarkers in older adults, they discovered distinct but additive effects of CeVD and AD-related markers on cognition and brain atrophy. CeVD acts as a global disruptor of brain communication networks, while AD markers, such as plasma p-tau181, follow separate pathways.

These findings emphasize the potential of combining neuroimaging and blood biomarkers for early detection and monitoring of dementia(Useless! Where is the prevention protocol? Oh, you incompetently haven't done that research?). The study provides new insights into the independent roles of CeVD and AD in driving cognitive and structural brain changes. Future research aims to refine brain connectivity markers for earlier predictions and targeted interventions.

Key Facts:

  • Dual Pathways: CeVD and AD markers independently and additively affect cognition and brain atrophy but do not synergize.
  • Brain Connectivity Impact: CeVD disrupts global brain network communication, influencing cognitive decline.
  • Predictive Biomarkers: Neuroimaging and blood-based markers show promise for early dementia risk assessments.

Source: NUS

Researchers have uncovered novel insights into how brain function disruptions related to cerebrovascular disease (CeVD) interact with Alzheimer’s disease (AD) pathology to impact neurodegeneration and cognition in older adults.

Led by Associate Professor Juan Helen Zhou, Director of the Centre for Translational Magnetic Resonance Research, Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), the research team revealed a brain functional connectome phenotype that is related to multiple CeVD markers and contributes additively to cognitive decline and neurodegeneration alongside AD.

This shows a brain.
While the two factors contributed additively to longitudinal cognitive decline and brain atrophy, the study found no evidence of a synergistic relationship between CeVD and p-tau181, suggesting that these factors may influence neurodegeneration in distinct pathways. Credit: Neuroscience News

The study highlights CeVD as a global disruptor of brain connectivity, reshaping our understanding of its role in dementia.

CeVD, often co-occurring with AD, has long been a significant area of study in ageing and dementia research. It refers to a group of conditions that affect the blood vessels and blood flow in the brain, such as stroke, cerebral atherosclerosis (narrowing or hardening of larger brain arteries due to plaque buildup), and small vessel disease that affects the tiny blood vessels in the brain.

These conditions can lead to brain damage by disrupting the delivery of oxygen and nutrients, which are essential for normal brain function.

In the study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, the team  examined the brain’s functional organisation in 529 older adult participants across the dementia spectrum, ranging from those with healthy cognition to individuals diagnosed with AD.

Analyzing how the different markers of CeVD and brain activity patterns correlate with affecting the participants, the team identified a global functional connectome phenotype, or a unique pattern in the brain’s communication network, that is strongly associated with high levels of the burden of four markers of CeVD seen on brain scans.

A key finding of the study was the identification of divergent effects of p-tau181, a blood-based biomarker for AD, and CeVD-related functional connectome phenotype on cognitive decline and brain atrophy.

While the two factors contributed additively to longitudinal cognitive decline and brain atrophy, the study found no evidence of a synergistic relationship between CeVD and p-tau181, suggesting that these factors may influence neurodegeneration in distinct pathways.

A/Prof Zhou said, “We discovered that a CeVD-related brain network phenotype, along with a key Alzheimer’s disease blood biomarker, can provide powerful insights into the future trajectory of cognitive decline and neurodegeneration.

“Our findings highlight the potential of brain connectome-based markers to track cognitive decline, particularly for individuals at-risk for dementia, and underscore the importance of integrating neuroimaging and blood biomarkers to better understand the pathophysiology of these co-occurring diseases.”

Dr Joanna Su Xian Chong, senior research fellow from A/Prof Zhou’s group, who is also first author of the study, added, “This pattern shows how the burden of multiple cerebrovascular disease markers can collectively exert widespread influences on brain function.

“Importantly, the combination of this pattern linked to CeVD and plasma p-tau181, a marker of Alzheimer’s disease, had independent and additive effects on long-term outcomes.

“Together, they contributed to cognitive decline and increased brain atrophy at baseline and over time, but did not interact directly to amplify each other’s effects.”

Both A/Prof Zhou and Dr Chong are also from the Centre for Sleep and Cognition and Healthy Longevity & Human Potential Translational Research Programmes at NUS Medicine.

Moving forward, the team aims to explore how the brain communication pattern linked to CeVD is affected by the severity, cause, and location of CeVD markers throughout the progression of the disease.

They also plan to investigate how this pattern interacts with different AD markers to contribute to brain degeneration and decline in multiple cognitive domains. Additionally, they aim to determine if these brain network features can be used as a reliable biomarker to monitor current and future cognitive decline, particularly in individuals at risk for dementia.

These features could offer more precise predictions than traditional brain imaging methods and help identify long-term cognitive outcomes earlier.

Their goal is to better understand the brain mechanisms behind CeVD and AD to develop advanced imaging tools for early detection and disease monitoring.

Funding: This research is supported by the National Research Foundation, Singapore under the NMRC Open Fund – Large Collaborative Grant (MOH-000500) and administered by the Singapore Ministry of Health through the NMRC Office, MOH Holdings Pte Ltd. 

Participants for the study were recruited from the National University Hospital and St Luke’s Hospital.

About this neuroscience research news

Author: Gladys Sim
Source: NUS
Contact: Gladys Sim – NUS
Image: The image is credited to Neuroscience News

Original Research: Open access.
Additive effects of cerebrovascular disease functional connectome phenotype and plasma p-tau181 on longitudinal neurodegeneration and cognitive outcomes” by Juan Helen et al. Alzheimer’s & Dementia

Thursday, May 5, 2022

New Research Identifies Blood Biomarker for Predicting Dementia Before Symptoms Develop

 

You better hope like hell your doctor has a protocol on testing for this post stroke and then has the protocols to prevent dementia.

New Research Identifies Blood Biomarker for Predicting Dementia Before Symptoms Develop

Researchers have identified a blood biomarker that could help identify people with the earliest signs of dementia, even before the onset of symptoms.

The findings were published in the Journal of Alzheimer’s Disease.

Emer McGrath, MD, College of Medicine Nursing and Health Sciences, National University of Ireland Galway, Galway, Ireland, and colleagues measured blood levels of P-tau181, a marker of neurodegeneration, in 52 cognitively healthy adults who were part of the US-based Framingham Heart Study, who later went on to have specialised brain positron emission tomography (PET) scans. The blood samples were taken from people who had no cognitive symptoms and who had normal cognitive testing at the time of blood testing.

The analysis found that elevated levels of P-tau181 in the blood were associated with greater accumulation of ß-amyloid on specialised brain scans. These scans were completed on average 7 years after the blood test.

Further analysis showed the biomarker P-tau181 outperformed t2other biomarkers in predicting signs of ß-amyloid on brain scans.

“The results of this study are very promising,” said Dr. McGrath. “P-tau181 has the potential to help us identify individuals at high risk of dementia at a very early stage of the disease, before they develop memory difficulties or changes in behaviour.”

The research team said the identification of a biomarker also points to the potential for a population screening programme.

“This study was carried out among people living in the community, reflecting those attending GP practices,” said Dr. McGrath. “A blood test measuring P-tau181 levels could potentially be used as a population-level screening tool for predicting risk of dementia in individuals at mid to late-life, or even earlier. This research also has important potential implications in the context of clinical trials. Blood levels of P-tau181 could be used to identify suitable participants for further research, including in clinical trials of new therapies for dementia. We could use this biomarker to identify those at a high risk of developing dementia but still at a very early stage in the disease, when there is still an opportunity to prevent the disease from progressing.”

Reference: https://content.iospress.com/articles/journal-of-alzheimers-disease/jad215639

SOURCE: National University of Ireland Galway


Friday, April 29, 2022

New Research Identifies Blood Biomarker for Predicting Dementia Before Symptoms Develop

 This originally came out in August 2021, what is the current status?

Blood Test Discerns Alzheimer's From Other Dementia With High Accuracy

With your good chance of getting dementia this test should be prescribed by your doctor to establish a baseline for you. And then if found implement THOSE EXACT DEMENTIA PREVENTION PROTOCOLS  your doctor should have competently already set up.

Your risk of dementia, has your doctor told you of this?

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

 

The latest here:

New Research Identifies Blood Biomarker for Predicting Dementia Before Symptoms Develop

Researchers have identified a blood biomarker that could help identify people with the earliest signs of dementia, even before the onset of symptoms.

The findings were published in the Journal of Alzheimer’s Disease.

Emer McGrath, MD, College of Medicine Nursing and Health Sciences, National University of Ireland Galway, Galway, Ireland, and colleagues measured blood levels of P-tau181, a marker of neurodegeneration, in 52 cognitively healthy adults who were part of the US-based Framingham Heart Study, who later went on to have specialised brain positron emission tomography (PET) scans. The blood samples were taken from people who had no cognitive symptoms and who had normal cognitive testing at the time of blood testing.

The analysis found that elevated levels of P-tau181 in the blood were associated with greater accumulation of ß-amyloid on specialised brain scans. These scans were completed on average 7 years after the blood test.

Further analysis showed the biomarker P-tau181 outperformed t2other biomarkers in predicting signs of ß-amyloid on brain scans.

“The results of this study are very promising,” said Dr. McGrath. “P-tau181 has the potential to help us identify individuals at high risk of dementia at a very early stage of the disease, before they develop memory difficulties or changes in behaviour.”

The research team said the identification of a biomarker also points to the potential for a population screening programme.

“This study was carried out among people living in the community, reflecting those attending GP practices,” said Dr. McGrath. “A blood test measuring P-tau181 levels could potentially be used as a population-level screening tool for predicting risk of dementia in individuals at mid to late-life, or even earlier. This research also has important potential implications in the context of clinical trials. Blood levels of P-tau181 could be used to identify suitable participants for further research, including in clinical trials of new therapies for dementia. We could use this biomarker to identify those at a high risk of developing dementia but still at a very early stage in the disease, when there is still an opportunity to prevent the disease from progressing.”

Reference: https://content.iospress.com/articles/journal-of-alzheimers-disease/jad215639

SOURCE: National University of Ireland Galway


Thursday, August 26, 2021

Blood Test Discerns Alzheimer's From Other Dementia With High Accuracy

With your good chance of getting dementia this test should be prescribed by your doctor to establish a baseline for you. And then if found implement THOSE EXACT DEMENTIA PREVENTION PROTOCOLS  your doctor should have competently already set up.

Your risk of dementia, has your doctor told you of this?

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 

The latest here:

Blood Test Discerns Alzheimer's From Other Dementia With High Accuracy

Plasma p-tau moves another step closer to clinical use

A technician prepares blood samples for mass spectrometry

Two blood markers, phosphorylated tau 217 (p-tau217) and phosphorylated tau 181 (p-tau181), showed strong diagnostic performances for Alzheimer's disease and discriminated Alzheimer's from frontotemporal lobar denervation (FTLD) syndromes and normal cognition, a retrospective study showed.

Both plasma biomarkers distinguished Alzheimer's disease syndromes from non-Alzheimer's disease disorders with a receiver operating characteristic area under the curve (AUC) greater than 0.90, reported Adam Boxer, MD, PhD, of the University of California San Francisco (UCSF), and colleagues, in Lancet Neurology.

"This confirms and extends our and others' previous work showing the exquisite sensitivity and specificity of new blood tests for Alzheimer's disease as opposed to other dementias," Boxer told MedPage Today.

"A previous JAMA manuscript suggested that plasma p-tau217 was highly superior to plasma p-tau181, however that study used two different types of tests which may have confounded the results," Boxer said. "Here, we used specially designed blood tests that differed only in their ability to detect either p-tau181 or 217. With these new tests, we show that both tests are highly accurate for diagnosis of Alzheimer's disease, although p-tau217 had small but statistically significant numerical advantages, for example in how well it correlated with tau-sensitive PET scans."

In the past 5 years, much research has focused on blood as a new matrix for Alzheimer's biomarkers that already had been validated in cerebrospinal fluid, noted Lucilla Parnetti, MD, PhD, of the University of Perugia in Italy, and colleagues, in an accompanying editorial.

"This study contributes substantially to the research of blood biomarkers for the diagnostic work-up of neurodegenerative diseases leading to dementia, by confirming the potential of plasma p-tau181 and p-tau217 for differential diagnosis," the editorialists wrote.

Boxer and colleagues studied 593 people, including 443 patients from the UCSF Memory and Aging Center and 150 patients from the Advancing Research and Treatment for Frontotemporal Lobar Degeneration Consortium in the U.S. and Canada. Mean age of the group was 64 and 50% were women. Data were collected between July 1 and Nov. 30, 2020, and immunochemical properties of p-tau217 and p-tau181 assays were directly comparable.

The cohort included 75 people who had been diagnosed with Alzheimer's disease syndromes (Alzheimer's disease dementia, logopenic variant primary progressive aphasia, posterior cortical atrophy), 99 people with mild cognitive impairment, 274 people with FTLD syndromes (corticobasal syndrome, progressive supranuclear palsy, behavioral variant frontotemporal dementia, non-fluent variant primary progressive aphasia, and semantic variant primary progressive aphasia), 14 people with Lewy body dementia, 13 people with traumatic encephalopathy syndrome, and 118 cognitively unimpaired controls.

Plasma p-tau217 and p-tau181 were correlated (r 0.90, P<0.0001). Both p-tau217 and p-tau181 concentrations were increased in people with Alzheimer's syndromes compared with cognitively unimpaired controls, with plasma p-tau217 showing an AUC of 0.98 (95% CI 0.95–1.00) and p-tau181 an AUC of 0.97 (95% CI 0.94–0.99).

P-tau217 outperformed p-tau181 in differentiating people with Alzheimer's disease syndromes from people with FTLD syndromes; p-tau217 had an AUC of 0.93 (95% CI 0.91–0.96) and p-tau181 an AUC 0.91 (95% CI 0.88–0.94; Pdiff=0.01). Both p-tau species were increased in pathology-confirmed Alzheimer's disease compared with pathology-confirmed FTLD.

Plasma p-tau217 was a stronger indicator of amyloid-PET positivity (AUC 0.91) than p-tau181 (AUC 0.89). Tau-PET binding in the temporal cortex was more strongly associated with p-tau217 than p-tau181.

The study had several limitations, Boxer and colleagues acknowledged. In the FTLD group, p-tau217 and p-tau181 concentrations were very low, with 79 measurements below the lower limit of quantification for p-tau217. Because the study focused on differential diagnosis, a relatively small number of people with Alzheimer's disease syndromes were included in the study. The cohort was relatively young and provided little information about how plasma p-tau will perform in older age.

"The tests we used are still for research only but hopefully within a few years, some versions will be available clinically," Boxer said. "Our results show that a well-designed, clinical grade p-tau181 or 217 blood test is likely to be very useful in many research and clinical applications."

"We are living in an exciting era of biomarkers for neurodegenerative disorders and are close to being able to apply them in clinical routine," the editorialists noted. "Healthcare providers and policymakers should become aware of, and knowledgeable about, the importance of this matter to enable use of blood biomarkers for diagnosis of neurodegenerative diseases to become a clinical reality."

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study was funded by the NIH, State of California Department of Health Services, Rainwater Charitable Foundation, Michael J. Fox Foundation, Association for Frontotemporal Degeneration, and Alzheimer's Association.

Researchers disclosed relationships with NIH, Rainwater Charitable Foundation, Association for Frontotemporal Degeneration, Bluefield Project to Cure Frontotemporal Dementia, Alzheimer's Drug Discovery Foundation, Alzheimer's Association, Alector, AGTC, Arkuda, Arvinas, AZTherapies, GlaxoSmithKline, Oligomerix, Ono, Regeneron, Roche, Samumed, Stealth, Third Rock, Transposon, Wave, Biogen, Eisai, Denali, Wave, Samumed, Siemens Healthineers, Pinteon Therapeutics, CogRx, Fujirebio, AlzeCure, Brain Biomarker Solutions, AVID Radiopharmaceuticals, GE Healthcare, Pfizer, AC Immune, AlzPathway, Cerveau, Abcam, Axon, JOMDD/Shimadzu, Julius Clinical, Lilly, MagQu, Novartis, Siemens Healthineers, Simon Foundation, Cura Sen, Wave Neuroscience, Ionis Pharmaceuticals, Mangurian Foundation, Little Family Foundation, EIP Pharma, Life Molecular Imaging, and Johnson & Johnson. Two researchers were employees of Eli Lilly and Company, which is exploring commercial development opportunities for p-tau assays. Another researcher holds a patent related to reagents used in p-tau assays.

Parnetti and co-authors disclosed no relationships with industry.

 

Tuesday, March 31, 2020

Getting Closer to a Blood Test for Alzheimer’s Disease? Dr. Francis Collins, NIH director

You'll want this so you can use the Alzheimer prevention protocols your doctor has.

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

 

You can't use mine, I'm not medically trained, your doctors are much better; vetted and clinically tested. 

Dementia prevention 19 ways per Dean

The latest here:

Getting Closer to a Blood Test for Alzheimer’s Disease? Dr. Francis Collins, NIH director

As research on Alzheimer’s disease (AD) advances, a desperate need remains for an easy blood test to help diagnose the condition as early as possible. Ideally, such a test could also distinguish AD from other forms of dementia that produce similar symptoms. As published recently in Nature Medicine, an NIH-funded research team has designed a simple blood test that is on course to meet these criteria [1].
The latest work builds on a large body of work showing that one secret to predicting a person’s cognitive decline and treatment response in AD lies in a protein called tau. Using the powerful, but expensive, approach of PET scan imaging, we know that tau builds up in the brain as Alzheimer’s disease progresses. We also know that some tau spills from the brain into the bloodstream.
The trouble is that the circulating tau protein breaks down far too quickly for a blood test to offer a reliable measure of what’s happening in a person’s brain. A few years ago, researchers discovered a possible solution: test for blood levels of a slightly different and more stable version of the protein called pTau181 [2]. (The “p” in its name comes from the addition of phosphorus in a particular part of the protein’s structure.)
In the latest study, researchers in the lab of Adam Boxer, University of California, San Francisco, followed up further on this compelling lead. Boxer’s team measured pTau181 levels in blood samples from 362 people between the ages of 58 and 70. Those samples included 56 people with an Alzheimer’s diagnosis, along with 47 people with mild cognitive impairment and 69 healthy controls.
The researchers also included another 190 people diagnosed with frontotemporal lobar degeneration (FTLD). It is a relatively rare form of dementia that leads to a gradual decline in behavior, language, and movement, often in connection with a buildup of tau in the brain.
The study found that levels of pTau181 were roughly 3.5-times higher in the blood of people with AD compared to people without AD. Those with mild cognitive impairment due to underlying AD also showed an intermediate increase in blood levels of pTau181.
Importantly, people with FLTD had normal blood levels of pTau181. As a result, the blood test could reliably distinguish between a person with AD and a person with FLTD. That’s important because, while FLTD is a relatively rare condition, its prevalence is similar to AD in people under the age of 65. But both conditions have similar symptoms, making it often challenging to distinguish them.
The findings add to evidence that the new blood test can help in diagnosing AD and in distinguishing it from other neurodegenerative conditions. In fact, it does so with an accuracy that often rivals more expensive PET scans and more invasive cerebrospinal fluid tests, which are now the only reliable ways to measure tau.
There’s still plenty of work to do before this blood test is ready for a doctor’s office. But these initial findings are very promising in helping to simplify the diagnosis of this devastating condition that now affects an estimated 5.5 million Americans [3].
References:
[1] Diagnostic value of plasma phosphorylated tau181 in Alzheimer’s disease and frontotemporal lobar degeneration. Thijssen EH, La Joie R, Wolf A, Strom A, Wang P, Iaccarino L, Bourakova V, Cobigo Y, Heuer H, Spina S, VandeVrede L, Chai X, Proctor NK, Airey DC, Shcherbinin S, Duggan Evans C, Sims JR, Zetterberg H, Blennow K, Karydas AM, Teunissen CE, Kramer JH, Grinberg LT, Seeley WW, Rosen H, Boeve BF, Miller BL, Rabinovici GD, Dage JL, Rojas JC, Boxer AL; Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators. Nat Med. 2020 Mar 2.
[2] Plasma phospho-tau181 increases with Alzheimer’s disease clinical severity and is associated with tau- and amyloid-positron emission tomography. Mielke MM, Hagen CE, Xu J, Chai X, Vemuri P, Lowe VJ, Airey DC, Knopman DS, Roberts RO, Machulda MM, Jack CR Jr, Petersen RC, Dage JL. Alzheimers Dement. 2018 Aug;14(8):989-997.
[3] Alzheimer’s Disease Fact Sheet. National Institute on Aging, May 22, 2019.

Monday, March 16, 2020

New blood test method may predict Alzheimer's disease

You likely will want this so you can get Alzheimer's prevention protocols from your doctor.  Assuming your doctor is competent and started working on this years ago(May 2012). 

 I'm doing this.

Dementia prevention 19 ways

Don't follow me, I'm not medically trained.

 

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:

New blood test method may predict Alzheimer's disease


At a Glance

  • A new blood testing technique could help researchers detect Alzheimer’s disease prior to onset or in those showing early signs of dementia.
  • The approach could be less invasive and costly than current brain imaging and spinal fluid tests, enabling earlier treatments and testing of novel approaches.
Older man getting blood drawn Researchers are working to develop a blood test for detecting Alzheimer’s disease that would be less invasive and costly than current approaches. Jovanmandic / iStock / Getty Images Plus
Alzheimer’s disease is an age-related brain disorder that develops over many years. Toxic changes in the brain slowly destroy memory and thinking skills. Symptoms most often first appear when people are in their mid-60s. The disorder gets worse over time and eventually leads to severe loss of mental function.
The process that destroys the brain involves two proteins called beta-amyloid and tau. Beta-amyloid clumps into plaques, which slowly build up between brain cells. Abnormal tau accumulates inside brain cells, forming tangles.
Researchers have found that PET scans of the brain and lab tests of spinal fluid can reveal disease-related changes, or pathology, twenty years before the onset of symptoms. Although the disorder is not reversable, early treatment may help preserve daily functioning for some time. Early diagnosis would also enable testing of novel drugs and other treatment approaches. However, PET imaging is expensive and involves radioactive agents, and spinal fluid tests are invasive, complex, and time-consuming. Researchers are looking for simpler, more cost-effective tests.
A team led by Dr. Adam Boxer at the University of California, San Francisco investigated whether a new blood testing technique called Simoa could be used to measure the concentrations of tau and predict development of Alzheimer’s disease. The study was funded in part by NIH's National Institute on Aging (NIA), National Institute of Neurological Disorders and Stroke (NINDS), and National Center for Advancing Translational Sciences (NCATS). Results were published online on March 2, 2020, in Nature Medicine.
The team collected blood samples from more than 400 people. They measured the concentration of ptau181—a modified version of tau that’s been linked with Alzheimer’s disease—in blood plasma, the liquid part of blood. Their analysis showed that the ptau181 in plasma differed between healthy participants and those with Alzheimer's pathology confirmed in autopsies. The test could also differentiate Alzheimer’s pathology from a group of rare neurodegenerative diseases known collectively as frontotemporal lobar degeneration.
The results with the plasma ptau181 test also mirrored results with two established biomarker tests for Alzheimer’s—a spinal fluid ptau181 test and a PET brain scan for beta-amyloid protein.
A research team in Sweden reported similar findings in a second paper published in the same journal issue. Using the same plasma ptau181 test, they were able to differentiate between Alzheimer's and other neurodegenerative diseases nearly as well as they could with a spinal fluid ptau181 test and a PET brain scan for tau protein. In addition, they followed participants for several years and observed that high levels of plasma ptau181 among those who were cognitively normal or had mild cognitive impairment could be used to predict later development of Alzheimer's dementia.
“The considerable time and resources required for screening research participants with PET scans and spinal taps slow the pace of enrollment for Alzheimer’s disease treatment studies,” says NIA Director Dr. Richard J. Hodes. “The development of a blood test would enable us to rapidly screen a much larger and more diverse group of volunteers who wish to enroll in studies.”