Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,245 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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 alzheimers test. Show all posts
Showing posts with label alzheimers test. Show all posts
PrecivityAD2 is the first blood-based biomarker for people as young as 40 with cognitive symptoms
The FDA cleared the PrecivityAD2 blood test to help diagnose Alzheimer's disease as part of a standard clinical workup, C2N Diagnostics announced Thursday.
The test, which measures plasma amyloid beta and tau peptide ratios to assess the likelihood of brain amyloid plaques, is the first Alzheimer's blood-based biomarker for people as young as 40 with cognitive symptoms.
PrecivityAD2 is indicated for adults with signs or symptoms of cognitive impairment being evaluated for Alzheimer's or other forms of cognitive decline. It's intended to be used with a clinical assessment to help healthcare professionals identify patients with amyloid pathology, not as a screening or standalone diagnostic test.
The test uses high-resolution mass spectrometry to quantify Alzheimer's disease biomarkers in blood, producing an outcome called the amyloid probability score 2 (APS2). The APS2 incorporates the ratio of plasma phosphorylated tau 217 (p-tau217) relative to non-p-tau217, combined with a plasma amyloid-beta 42/40 ratio, to rule in or rule out Alzheimer's disease.
In a validation study of 1,142 people with signs or symptoms of cognitive decline, PrecivityAD2 showed a 97.6% positive predictive value (rule-in) and a 93.1% negative predictive value (rule-out) to detect brain amyloid plaques using dual cutoffs measured against amyloid PET or cerebrospinal fluid testing, C2N reported. The test was effective at detecting plaques in a wide range of patients, including people with mild symptoms and those with more advanced cognitive impairment.
PrecivityAD2 showed consistent diagnostic performance as age increased and in people with comorbidities like atrial fibrillation, autoimmune or inflammatory disease, chronic heart failure or kidney disease, coronary heart disease, depression, diabetes, dyslipidemia, history of cancer, history of stroke or transient ischemic attack, hypertension, or obesity, the company added.
A recent study in Sweden showed the test was useful to help primary care physicians rule out Alzheimer's disease. Earlier research showed the APS2 score performed better than primary care doctors or dementia specialists in detecting Alzheimer's disease among people with cognitive symptoms.
In 2025, the FDA cleared two other diagnostic blood tests for Alzheimer's disease: one to help clinicians identify Alzheimer's in people with signs and symptoms, the other to rule out Alzheimer's disease in primary care.
Lab-developed tests not approved by the FDA are also on the market. Last year, the Alzheimer's Association issued guidance outlining sensitivity and specificity parameters for Alzheimer's blood tests to either triage or diagnose people with cognitive impairment.
An estimated 19 to 20 million U.S. adults 65 and older, and hundreds of thousands more between the ages of 45 and 65, have cognitive impairment and may benefit from an early diagnosis, C2N Diagnostics noted.
PrecivityAD2 can be ordered by healthcare professionals experienced in evaluating patients with cognitive impairment, the company stated. It currently is available as a lab-developed test; the FDA-cleared test version is expected to be available later this year.
A self-administered, in-home, finger-stick blood test detected Alzheimer's disease (AD) biomarkers that correlated with cognitive performance in older adults — a finding that could open the door to large-scale dementia risk screening outside of clinical settings.
The cross-sectional observational validation study of 174 participants (mean age, 66 years; 54% female) showed capillary blood levels of p-tau217 correlated with episodic memory, attention, and executive function, while glial fibrillary acidic protein (GFAP) correlated with working memory and executive function, as measured by computerized cognitive tests.
When researchers combined the p-tau217 results with composite memory scores, they identified a high-risk group — about 9% of participants — who performed significantly worse across cognitive and functional measures.
The approach is designed to move AD biomarker testing out of specialist clinics and into the community, where most people with early cognitive concerns are never evaluated.
"This is the whole reason for doing the capillary blood sampling — to allow it to be scalable, to allow it to be done at a community level, which is where it's likely to be most usefully employed," study investigator Anne Corbett, PhD, professor in dementia research at the University of Exeter Medical School, Exeter, England, told Medscape Medical News.
The study builds on the DROP-AD trial, which validated capillary blood sampling for AD biomarkers in 337 participants.
As reported previously by Medscape Medical News, that study demonstrated strong concordance between capillary and venous samples — but collection was still supervised in clinical settings. In the current study, participants collected samples entirely at home and returned them by mail.
In the UK, only 1 in 1000 people with early cognitive decline receive a specialist evaluation. Corbett said the study deliberately set its memory threshold at 1 SD below age-matched norms — milder than the 1.5 SD cutoff for mild cognitive impairment — to catch people earlier in the disease course.
"When you look at the new generation of disease-targeted treatments, they are looking for preclinical mild cognitive impairment with biomarkers," she said. "That's even more relevant in the US, where some of these drugs are already in use."
Participants were either cognitively normal (n = 146) or had mild to moderate dementia (n = 28). Each collected 70 μL of capillary blood using a Capitainer dried blood spot device. Cards were dried at room temperature and mailed without cooling.
Capillary p-tau217 correlated with episodic memory (r = 0.299; P < .001), attention (r = 0.197; P = .019), and executive function (r = 0.191; P = .021). GFAP correlated with working memory (r = 0.183; P = .034) and executive function (r = 0.182; P = .046).
Both biomarkers discriminated between participants with and without dementia, though with modest accuracy (p-tau217 AUC = 0.656, P = .012; GFAP AUC = 0.688, P < .001). The high-risk group identified through the dual-threshold approach showed large effect sizes across cognitive and functional domains (Cohen d > 1.0).
In a subgroup of 40 participants with paired venous samples, capillary-venous correlations were strong (p-tau217: r = 0.711-0.743; GFAP: r = 0.700-0.790).
An unexpected finding was that only 6% of participants were positive for both biomarkers. GFAP-positive participants were nearly five times more likely to report a history of heart disease (odds ratio, 4.14; P = .016), while p-tau217 positivity had no cardiovascular association, suggesting the two markers may identify distinct at-risk populations.
"We didn't expect quite such a separation," Corbett said. She described the finding as exploratory and said her group planned to examine whether the two groups showed different cognitive trajectories.
Corbett estimated a timeline of 4 to 5 years before the approach could enter clinical pathways and said her group was launching a study this summer to prototype the technology in a real-world NHS context.
Foundational Research
Commenting for Medscape Medical News, Suzanne Schindler, MD, PhD, associate professor of neurology at Washington University School of Medicine, St. Louis, Missouri, said the study addressed a real problem but that the data supported feasibility, not clinical readiness.
"This isn’t ready for clinical practice, but it's laying groundwork for future studies," Schindler said.
She noted the cohort lacked a dedicated mild cognitive impairment (MCI) group, making it difficult to assess the tool's effectiveness in a population it seemed designed to reach. "They likely will be able to identify some of the individuals at highest risk and lowest risk, but there's going to be a lot of people that aren't stratified," said Schindler, who was not involved in the study. "It has value for the extremes, but for those folks in the middle, it's not going to stratify them."
Schindler differentiated this approach from a previous direct-to-consumer blood biomarker test by Quest Diagnostics that drew criticism for high false-positive rates. That test used the amyloid-beta 42-to-40 ratio, which was less specific, and was framed as a clinical tool. The current study's higher-specificity cutoff and triaging framing made it less concerning, she said.
She noted that blood biomarker testing is recommended only for symptomatic individuals, in part because approved treatments target people who already have cognitive impairment. But trials are underway testing anti-amyloid therapies in people with no symptoms.
"If that happens, we will then have a need to screen people who are cognitively unimpaired," she said, a scenario that would make scalable, home-based testing far more urgent.
Marwan Sabbagh, MD, professor of neurology and Moreno Family Chair for Alzheimer's Research at the Barrow Neurological Institute, Phoenix, Arizona, who was also not involved in the research, said the sample needed to be much larger and more diverse. "You need a bigger spread. … You need more MCI," Sabbagh told Medscape Medical News.
But Sabbagh did see major potential in getting at-risk individuals into the clinical pathway more quickly than what’s traditionally done.
"A typical 70-year-old goes to primary care, and primary care may or may not screen them, may or may not evaluate them, and may or may not refer them," he said. Capillary testing could compress that timeline dramatically — flagging at-risk individuals through an online cognitive test, sending a kit in the mail, and returning a result in days rather than months.
He added that capillary testing could eventually replace venous plasma testing as a gating mechanism before PET scans, but he said the field was not ready for a direct-to-consumer model.
"This could become part of the annual Medicare wellness visit," Sabbagh said. "I'm not sure we're ready to jump to a direct-to-consumer model."
The study was funded by the National Institute for Health and Care Research Invention for Innovation program and the NIHR Exeter Biomedical Research Centre. Disclosure information for study authors is available in the original study publication. Schindler reported no relevant financial relationships.
Because of your extra risk of dementia post stroke, you'll want this test so your doctor CAN IMPLEMENT THOSE EXACT ALZHEIMER'S PREVENTION PROTOCOLS THAT WERE WRITTEN AGES AGO! Oh NO, your doctor failed at that! Well, you're screwed, but your doctor is still getting paid for incompetence!
Let's check the other Alzheimer's testing available from your competent? doctor! Oh, NOTHING EXISTS IN YOUR HOSPITAL?
A quick, outpatient nasal swab can detect early biological changes linked to Alzheimer’s disease (AD) years before cognitive or memory symptoms present.
Sampling cells in the upper nasal cavity via a minimally invasive brush biopsy may be able to detect AD years before symptoms appear.
Investigators analyzed brush biopsy samples from the olfactory cleft — the narrow upper region of the nasal cavity that houses the olfactory epithelium — and identified immune and neuronal changes that mirror those seen in the brains of people with AD. These signatures distinguished individuals with preclinical and clinical AD from healthy control individuals.
“The nasal biopsy approach is still a research tool rather than something ready for routine care,” study investigator Vincent D’Anniballe, an MD-PhD student with the medical scientist training program at Duke University in Durham, North Carolina, told Medscape Medical News.
“Potentially,” said D’Anniballe, “because the sampling can be repeated and gives us a window into living nerve and immune cells, it could one day help track whether a treatment is changing Alzheimer’s-related biology over time.”
The study was published online on March 18 in Nature Communications.
A Window Into Central Neuropathology
Loss of smell is one of the earliest signs of AD. The olfactory epithelium — located in the upper nasal cavity — harbors olfactory sensory neurons that can accumulate hallmark AD pathology, including amyloid-beta plaques and neurofibrillary tangles, suggesting the olfactory epithelium may “faithfully mirror central AD neuropathology,” the researchers wrote.
To investigate, they profiled olfactory epithelium brush biopsies obtained from healthy control individuals, individuals with cerebrospinal fluid (CSF) biomarker-confirmed AD, and cognitively typical individuals whose positive CSF biomarkers signal a preclinical AD stage.
The biopsy results revealed a “continuum of disease-linked shifts detectable in biomarker-positive, cognitively unimpaired patients and mirrored in the clinical AD.”
Activated CD8 memory T cells and inflammatory myeloid programs were present in adults with preclinical AD and were also present — often at greater magnitude — in adults with clinical AD.
In addition, olfactory sensory neurons in adults with preclinical and clinical AD showed stress-related transcriptional signatures that mirrored those previously reported in postmortem AD brains, suggesting that the olfactory epithelium reflects disease activity occurring deeper in the brain.
A combined gene-expression score derived from the olfactory biopsies was able to distinguish individuals with preclinical and clinical AD from healthy control individuals with about 81% accuracy.
“At this point, our study cannot separate cause from effect. The fact that we see immune cell changes so early suggests they may be a part of the disease process, but we still need follow-up studies to know whether they are driving the disease or reacting to it,” D’Anniballe noted.
Looking ahead, the researchers plan to expand their work to larger patient groups and explore whether olfactory brush biopsy could be used to monitor disease progression or response to therapy over time.
“The biggest hurdles are proving in larger studies that it is reliable and scalable before it can work as a practical clinical test,” said D’Anniballe.
A ‘Compelling’ Early Signal
Reached for comment, Sheena Aurora, MD, vice president of medical affairs at the Alzheimer’s Association, said the results are “intriguing,” given that loss of smell is one of the first symptoms of AD in some people and “targeting the olfactory epithelium is a novel approach.”
However, she noted that the study is very small and preliminary. As a result, the findings need to be replicated and confirmed in larger, more representative study populations before the technique could be considered clinically viable.
Another study limitation is the fact that olfactory cleft biopsies have highly variable rates of success, said Aurora, who wasn’t involved in the research.
If it is eventually validated, this approach could help support diagnosis alongside existing amyloid and tau measures, guide the selection and monitoring of patients for disease-modifying therapies, and provide a way to study early AD-related changes in the brain and adjacent tissues, she noted.
Also weighing in on the findings, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, said this study “turns the nose into a window into the brain. For the first time, we’re seeing Alzheimer’s biology unfold in living neural tissue before symptoms even begin.”
“What’s striking is that the inflammatory signature of Alzheimer’s is already present in people who are cognitively normal. That fundamentally shifts how we think about when this disease begins,” said Lakhan, who was not involved in the research.
“The olfactory epithelium is one of the only places where you can safely sample living human neurons. That’s been the missing piece in Alzheimer’s research. This is not a nasal swab. It’s a targeted biopsy of olfactory neural tissue, which is why it captures real brain biology, not just surface signals,” he added.
Lakhan said the findings point to a potential pharmacodynamic biomarker, offering a way to directly observe how interventions — whether drugs or digital therapeutics — affect neural and immune pathways in living human tissue.
If validated, he added, the approach could transform early detection and clinical trials by providing an earlier, biologically grounded signal of disease activity and treatment response.
He emphasized, however, that the work remains an early proof-of-concept, albeit with a strong and biologically coherent signal.
Funding for the study was provided by the National Institutes of Health. D’Anniballe reported having no disclosures. Duke University and four authors are named inventors on a US patent application related to methods for obtaining olfactory cleft brush biopsy samples and measuring gene-expression biomarker panels to detect/diagnose and guide treatment of preclinical AD. Aurora and Lakhan reported having no relevant disclosures.
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
Plasma eMTBR-tau243 also could help identify people with high tau burden
Key Takeaways
Alzheimer's can be detected early with p-tau blood biomarkers, but some tests can lead to overdiagnosis.
Combining p-tau217 and eMTBR-tau243 may refine diagnostic accuracy and reduce false-positives.
Plasma eMTBR-tau243 also could help identify people with high tau burden.
A combination of two blood tests improved Alzheimer's disease triaging and reduced overdiagnosis in people with asymptomatic Alzheimer's pathology, a prospective cohort study showed.
Together, the two tests -- one assessing the ratio of phosphorylated tau 217 to non-phosphorylated tau (%p-tau217), the other measuring microtubule-binding region-tau243 (eMTBR-tau243) -- identified people with established Alzheimer's disease with an accuracy of 81%, a positive predictive value (PPV) of 84%, a negative predictive value (NPV) of 77%, and a sensitivity of 82%, reported Niklas Mattsson-Carlgren, MD, PhD, of Lund University in Sweden, and co-authors.
Positive eMTBR-tau243 was associated with worse longitudinal cognitive decline and longitudinal tau tangle accumulation in p-tau217-positive patients. In this group, eMTBR-tau243 had an accuracy of 87%, a PPV of 76%, and an NPV of 90% for identifying individuals with high tau-PET load, Mattsson-Carlgren and colleagues said in Lancet Neurology.
The proportion of false-positive test results for established Alzheimer's disease fell from 43% with %p-tau217 alone to 16% with %p-tau217 and eMTBR-tau24 combined, the researchers noted.
Two-step testing, with %p-tau217 as an initial test to identify Alzheimer's pathology followed by eMTBR-tau243, could refine diagnostic accuracy, Mattsson-Carlgren and colleagues suggested. Plasma eMTBR-tau243 also could help identify individuals with high tau burden who might have less benefit from amyloid-targeting therapies.
"Plasma p-tau217 is excellent to identify presence of amyloid pathology, which is a core feature of Alzheimer's disease. But amyloid pathology presents early, before clinical symptoms. By combining p-tau217 with eMTBR-tau243, which increases later in disease, in correlation with aggregated tau pathology, we can increase our confidence that Alzheimer's is not only present, but also contributes to symptoms," Mattsson-Carlgren told MedPage Today.
"Individuals with isolated increased p-tau217 without increased eMTBR-tau243 may be more likely to have Alzheimer's in very early stage, without clear relevance to the current symptoms," he pointed out.
"This type of fine-grained understanding of how different aspects of Alzheimer's disease are present and explain symptoms has not been possible with blood tests before," he added. "If these methods can be used in clinical practice, it will enable objective biological staging of Alzheimer's, which can guide patient management."
Plasma p-tau217 can reflect abnormal amyloid pathology decades before Alzheimer's symptom onset, but also can be abnormal when amyloid is a co-pathology in other diseases, noted Nicholas Ashton, PhD, of Banner Alzheimer's Institute in Phoenix.
"Therefore, interpretation of p-tau217 in isolation might increase the risk of overdiagnosis, especially in a preclinical population or when amyloid pathology is not the primary driver of the clinical syndrome," Ashton wrote in an accompanying editorial.
A growing demand for fast diagnostic testing coupled with the need for sufficient accuracy is a fundamental challenge facing the Alzheimer's field, Ashton observed. "Blood biomarkers clearly address the former, but their ability to reliably inform clinical care remains under scrutiny, despite recent regulatory approvals," he said.
A sequential framework of p-tau217 and eMTBR-tau243 tests could move the field toward biologically informed diagnosis and stratification, he pointed out. "As disease-modifying treatments become more available, the ability to distinguish early amyloid positivity from tau-driven symptomatic disease will be essential, not only for treatment selection, but also for avoiding both overdiagnosis and missed opportunities for timely intervention," Ashton wrote.
Mattsson-Carlgren and co-authors evaluated 572 adults with cognitive symptoms -- 142 participants with subjective cognitive decline, 259 with mild cognitive impairment, and 171 with dementia -- in the Swedish BioFINDER 2 study. About half (51%) were female.
Overall, 350 people had positive plasma %p-tau217. Of these, 341 people (97%) were amyloid-positive by cerebrospinal fluid biomarkers or PET. Just over half -- 194 of 350 participants (55%) -- also were positive for eMTBR-tau243.
The overall findings were validated in an independent cohort of both cognitively impaired and unimpaired patients from the Knight Alzheimer Disease Research Center (ADRC) at Washington University in St. Louis, the researchers said.
The study has several limitations, they acknowledged. The main sample was made up of Swedish participants, though results were consistent in the Knight ADRC cohort. Cross-validation in other populations and primary care settings is essential, they added.
The eMTBR-tau243 marker also needs further work, Mattsson-Carlgren noted. "The next step is to investigate whether the test can be simplified, and whether it can be used more widely -- in primary care, for example," he stated.
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. Connect:
Disclosures
This study was supported by the National Institute of Aging, European Research Council, Alzheimer's Association, GHR Foundation, Swedish Research Council, ERA PerMed, Knut and Alice Wallenberg Foundation, Strategic Research Area MultiPark at Lund University, Swedish Alzheimer Foundation, Swedish Brain Foundation, Parkinson Foundation of Sweden, Cure Alzheimer's Fund, Rönström Family Foundation, Berg Family Foundation, Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, Skåne University Hospital Foundation, Michael J. Fox Foundation, Lilly Research Award Program, Regionalt Forskningsstöd, Wallenberg AI, Autonomous Systems and Software Program and Data-Driven Life Science, Greta and Johan Kock Foundation, and the Swedish federal government.
Mattsson-Carlgren received consultancy or speaker fees from BioArctic, Biogen, Eli Lilly, Merck, Novo Nordisk, Roche, and Owkin. Co-authors reported relationships with pharmaceutical companies and other groups.
Ashton reported relationships with AbbVie, Athira, ImaginationLand, MapLight Therapeutics, Spear Bio, Neurogen Biomarking, Quanterix, TauRx, Eli Lilly, Roche, Beckman Coulter, Janssen, Bristol Myers Squibb, ImmunoBrain, Alamar Biosciences, Biogen, and VJDementia.
New research provides more evidence that dried blood samples collected from a simple finger prick can be used to measure key biomarkers of Alzheimer’s disease (AD).
In a multicenter study of more than 300 participants, levels of p-tau217 in finger-prick samples closely matched results from standard blood tests, and they could identify AD-related changes in spinal fluid with an accuracy of 86%.
“These findings underscore the potential of dried blood collection and capillary blood as a minimally invasive, scalable approach for AD biomarker testing in research settings. Yet, further refinement of collection and analytical protocols is needed to fully translate this approach to be viable and useful as a clinical tool,” the investigators cautioned.
For now, “what we have shown is that it’s an extremely useful research tool, and we already have large scale research studies going on, but we don’t envision this anytime soon to be a clinical test,” Nicholas Ashton, PhD, senior director of the Banner Fluid Biomarker Program, Banner Sun Health Research Institute in Sun City, Arizona, told Medscape Medical News.
The study was published online on January 5 in Nature Medicine. A Close Match
Blood biomarkers, p-tau217 in particular, have emerged as accurate tools for detecting AD pathology, offering a minimally invasive alternative to PET or lumbar puncture. Yet, standard blood testing still depends on venipuncture, controlled processing, and trained personnel, limiting scalability.
The DROP-AD project is evaluating whether AD biomarkers can be reliably measured from dried blood spot or dried plasma spot, derived from capillary blood obtained via finger prick, for detecting AD biomarkers, including p-tau217, glial fibrillary acidic protein (GFAP), and neurofilament light (NfL).
The current study included 337 participants recruited across seven European centers, spanning cognitively normal individuals, patients with mild cognitive impairment, AD dementia, non-AD dementias, and individuals with Down syndrome. A total of 304 participants provided paired capillary dried plasma or blood spot samples, as well as venous plasma samples.
Levels of p-tau217 in the finger-prick samples closely matched results from standard venous blood samples (Spearman’s rank correlation coefficient = 0.74; P < .001).
Dried plasma spot p-tau217 levels increased progressively across clinical disease stages and showed “good accuracy” in predicting CSF biomarker positivity, with an area under the curve of 0.864.
Home-Based Sampling?
The investigators also successfully detected GFAP and NfL from dried blood and plasma spot analysis.
“Both GFAP and NfL showed high concordance between capillary and venous samples, and were similarly associated with cognitive performance and age, reinforcing the validity of these remote sampling methods,” the authors reported.
Notably, the study also demonstrated feasibility in individuals with Down syndrome, a population at high genetic risk for AD for whom venipuncture can be particularly challenging.
In the subgroup with Down syndrome, capillary biomarker concentrations were higher in those with dementia than in asymptomatic individuals and showed strong agreement with venous plasma levels.
The study also found “high concordance” between supervised and unsupervised blood collections, suggesting that remote or home-based sampling may be feasible.
Not Ready for Clinical Use
The findings build on earlier data from the DROP-AD project, as reported by Medscape Medical News.
“Despite the promise shown, we do not currently recommend the use of dried blood analysis for clinical use, decision-making, or patient management because of observed differences in analytical performance and diagnostic accuracy between capillary-derived and venous blood samples,” the authors cautioned.
Further methodological refinement, standardization, and validation in larger cohorts are required before this approach can be translated into routine clinical practice, they concluded.
Once that happens, Ashton said he could envision a “scenario in the future” where elderly asymptomatic individuals could be sent a dried blood spot card as a “first step in triage.”
“Especially if we get a readout next year, or even this year, that antiamyloid drugs are beneficial to people without symptoms because these individuals are not going to be walking into our clinics in primary care or specialty services because they don’t have objective memory concerns,” Ashton said.
Having an at-home test could help engage asymptomatic people with positive biomarkers in early treatment, he added.
Worth Further Study
Reached for comment, Maria C. Carrillo, PhD, Alzheimer’s Association chief science officer and medical affairs lead, said blood-based biomarkers are “reshaping how we identify, diagnose, and understand Alzheimer’s disease, especially in research settings.”
“Currently, the evidence supports the use of blood biomarkers as one tool of many in a multi-phase diagnostic process in people experiencing changes in memory and thinking abilities. The science is not yet strong enough to recommend blood tests as a standalone diagnostic, nor for their use in people without symptoms,” Carrillo told Medscape Medical News.
The association’s clinical practice guideline provides clear, evidence-based recommendations for when and how blood-based biomarker tests can be responsibly integrated into diagnostic workflows in specialty care, she noted.
Carrillo said the Alzheimer’s Association “agrees with the authors that more research is needed before this [finger-prick] technique can become a suitable tool for clinicians.”
However, the finding that the biomarker results were very similar between the supervised and self-collected blood samples “shows that the idea has merit and is worth further investigation — in a variety of locations and situations, and with much larger and more representative populations — to help ensure that the test results are credible and consistent wherever they are done.”
Summing up, Carrillo said, “The approach described in this new paper points to a future where Alzheimer’s biomarker testing is simple, minimally invasive, widely available, and potentially even self-administered.”
The study had no commercial funding. Ashton reported receiving consultancy and/or speaker fees from Alamar Biosciences, BioArctic, Biogen, Eli Lilly, Neurogen Biomarking, Roche, Spear Bio, Quanterix, and Vigil Neuroscience. A complete list of author disclosures is provided with the original article. Carrillo had no relevant disclosures.
Isn't your competent? doctor already testing you with the 2 Finger Test In Dementia? and you correctly declined it since your stroke deficits bias the test. Declining it proves you don't have dementia since you know of the bias.
A mail-in pinprick blood test accurately detects markers of Alzheimer’s disease
The test’s results mirrored those from standard blood and spinal fluid tests
The test evaluates dried blood samples dripped onto a card
TUESDAY, Jan. 6, 2026 (HealthDay News) — A mail-in blood test accurately detects markers linked to Alzheimer’s disease, potentially making the degenerative brain condition easier to diagnose and research, a new study says.
The
finger-prick test accurately measures blood levels of tau proteins,
glial fibrillary acidic proteins and neurofilament light fragments,
researchers reported Jan. 5 in the journal Nature Medicine.
All are hallmarks of brain damage associated with Alzheimer’s, researchers said.
The
test is still years away from clinical use among regular patients, but
currently could help fuel research efforts into Alzheimer’s, researchers
said.
“Ultimately, we are moving toward a pathway of treating
people for Alzheimer’s disease before symptoms emerge,” said senior
researcher Nicholas Ashton, senior director of Banner Health’s Fluid Biomarker Program in Sun City, Arizona.
“If
this trajectory continues, we will need innovative ways to identify
eligible individuals who are not routinely presenting in clinical
settings,” Ashton said in a news release. “This work represents one such
approach in that direction and further validation remains.”
For
the study, researchers analyzed dried blood samples provided by 337
people. Participants provided a few drops of blood, which were dried on a
card before lab analysis.
The lab work looked at blood levels of:
Phosphorylated tau proteins, which form toxic clumps in the brains of Alzheimer’s patients
Protein fragments of neurofilament light chain (NfL), which are released from damaged or dying brain cells
Glial Fibrillary Acidic Protein (GFAP), a protein produced by cells that heal and protect neurons in the brain and spinal cord
The pin-prick samples showed levels of tau proteins that closely matched those found in standard blood and spinal fluid tests.
The dried blood samples also accurately captured people’s levels of GFAP and NfL, researchers said.
This
simple technique could make it easier to perform large-scale
Alzheimer’s studies by enabling remote participation, researchers said.
“What excites me most is the democratization of biomarker research this enables,” Anne Corbett,
a professor of dementia research at the University of Exeter in the
U.K., said in a news release. “We’re moving toward a future where
anyone, anywhere, can contribute to advancing our understanding of brain
diseases. This isn’t just a technical advancement — it’s a paradigm
shift in how we conduct neuroscience research.”
This method also could help research efforts associated with other brain diseases, including Parkinson’s disease, multiple sclerosis, Amyotrophic Lateral Sclerosis (ALS) and brain injuries, researchers said.
