AI-Enabled Parkinson’s Disease Screening Using Smile Videos

 Will your competent? doctor get this as a screening tool for your risk of Parkinsons' post stroke? NO? So, you don't have a functioning stroke doctor, do you?

 Parkinson’s Disease May Have Link to Stroke March 2017  

The latest here:

AI-Enabled Parkinson’s Disease Screening Using Smile Videos

Authors: Adnan M.Sc. https://orcid.org/0000-0002-8012-6679 Islam M.Sc. https://orcid.org/0000-0003-3725-3493 Sangwu B.Sc. https://orcid.org/0000-0003-3930-3079 E.M. Ph.D. https://orcid.org/0000-0002-9736-442X Sutapa Dey Tithi B.Sc. https://orcid.org/0009-0007-5815-882X Kazi Noshin B.Sc. https://orcid.org/0009-0008-6015-8236 Md Rayhanul Islam M.Sc. https://orcid.org/0000-0001-8384-6180 Hoque Ph.D. https://orcid.org/0000-0003-4781-4733 Author Info & Affiliations Published  NEJM AI 2 NO.  7 Copyright © 2025 Information & Authors

Abstract

Background Parkinson’s disease (PD) diagnosis is challenging owing to insufficient access to clinical care. We present an efficient and accessible artificial intelligence–driven PD screening method leveraging the largest video dataset of facial expressions from 1452 unique participants, including 391 with PD — 300 of whom have been clinically diagnosed and 91 of whom self-reported the condition.

We recruited individuals across multiple countries — primarily North America — via social media, email outreach, and a PD research registry; patients undergoing in-person PD assessments at a U.S. clinic; clients of a U.S.-based PD wellness center and their caregivers; and individuals in Bangladesh identified as being at high risk for PD. Participants used an online tool to record themselves (either at home or in a clinical setting) mimicking three facial expressions (i.e., smile, disgust, and surprise). Facial landmarks and action unit–based features were extracted to quantify hypomimia. Machine-learning models were trained on these features to distinguish between individuals with and without PD. The model’s generalizability was tested on external test datasets (from the U.S. clinic and Bangladesh).ResultsAn ensemble of models trained on smile videos achieved an accuracy of 87.9 ± 0.1% and an area under the receiver operating characteristic curve (AUROC) of 89.3 ± 0.3% in 10-fold cross-validation, with a 76.8 ± 0.4% sensitivity, 91.4 ± 0.3% specificity, 73.3 ± 0.5% positive predictive value (PPV), and 92.7 ± 0.1% negative predictive value (NPV). On the U.S. clinic test set, it achieved an 80.3 ± 1.6% accuracy and an 83.3 ± 1.4% AUROC, with a 80.0 ± 2.5% sensitivity, and 80.5 ± 2.0% specificity. On the test set from Bangladesh, performance reached an 85.3 ± 1.4% accuracy with an 81.5 ± 1.8% AUROC. The specificity, sensitivity, and NPV remained competitive, while PPV declined to 35.7 ± 4.8%. No detectable bias was observed across sex and ethnic subgroups, except on the test dataset from Bangladesh, for which performance was significantly better for female participants.Conclusions Smiling videos can effectively differentiate between individuals with and without PD, offering a potentially easy, accessible, and cost-efficient way to screen for PD, especially when access to clinical diagnosis is limited. (Funded by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health number, P50NS108676 and others.)

Blood test detects Parkinson’s years before symptoms appear using RNA markers

 Is your doctor and hospital competent enough to get this installed as a protocol to detect your risk of Parkinsons post stroke and then implement the Parkinsons prevention protocols they should have, but don't?

Parkinson’s Disease May Have Link to Stroke March 2017 

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Blood test detects Parkinson’s years before symptoms appear using RNA markers

Scientists have developed a fast, non-invasive blood test that can detect Parkinson’s disease before tremors begin. By measuring RNA fragments that reflect brain pathology, the test offers new hope for early diagnosis and targeted intervention.

In a recent study published in the journal Nature Aging, researchers evaluated whether a blood test measuring nuclear and mitochondrial transfer RNA (tRNA) fragments could accurately detect pre-symptomatic Parkinson’s disease (PD).

Background

What if we could detect PD before a single tremor begins? PD is the second most common neurodegenerative disorder globally, affecting over 10 million people worldwide according to widely cited estimates and causing progressive movement and cognitive impairments. Current diagnostic methods are often reactive, identifying the disease after significant brain damage has already occurred. Invasive tests and inconsistent biomarkers further hinder early diagnosis. Transfer RNA fragments (tRFs), small non-coding RNA pieces generated by enzymatic cleavage, are emerging as potential indicators of neurological disorders. Their levels shift in response to mitochondrial dysfunction and neuronal stress, both hallmarks of PD. However, further research is needed to validate their diagnostic power.

About the Study

Patient-specific “fingerprints”: Blood tRF levels remained stable over time in individuals, creating unique molecular profiles that could enable personalized tracking of disease progression.

Researchers conducted a multi-cohort analysis using small RNA sequencing and quantitative polymerase chain reaction (qPCR) to explore the diagnostic potential of specific tRFs in PD. They analyzed cerebrospinal fluid, blood, and brain samples from patients with PD, Alzheimer’s disease, and healthy controls, including postmortem samples from the Netherlands Brain Bank (NBB) and living donors from the Parkinson’s Progression Markers Initiative (PPMI). The study focused on two tRF families: nuclear-originated RGTTCRA-tRFs, derived from transfer RNA and marked by a specific repetitive motif ([A/G]GTTC[A/G]A), and mitochondrial tRFs (MT-tRFs), originating from mitochondrial genomes. A ratio between the two was calculated to standardize differences across individuals.

Using the PPMI dataset, they evaluated this ratio in early-stage, mutation-carrying, and prodromal patients. Using dual qPCR, they also validated the findings in fresh blood samples (Shaare Zedek Medical Center cohort) and postmortem brain tissues (NIH NeuroBioBank). Furthermore, they used a gradient-boosted machine learning (GBM) model to compare the predictive accuracy of the tRF ratio to traditional clinical scores like the Unified Parkinson’s Disease Rating Scale (UPDRS) and the Hoehn and Yahr (H&Y) scale. Additional experiments included overexpression and knockout of angiogenin (ANG), a tRNA-cleaving enzyme, and ribosomal profiling to examine the biological effects of RGTTCRA-tRF accumulation on protein synthesis.

Study Results

The study revealed distinct changes in transfer RNA fragments associated with PD. In cerebrospinal fluid, patients exhibited elevated levels of RGTTCRA-tRFs and decreased levels of MT-tRFs compared to controls and individuals with Alzheimer’s disease. This unique tRF profile was consistent in both sexes and showed no overlap with Alzheimer’s disease signatures. Similarly, brain tissue from the substantia nigra (the region most affected in PD) showed high RGTTCRA-tRF levels correlating with the presence of Lewy bodies, protein aggregates that are a hallmark of the disease.

Mitochondrial tRNA collapse: Postmortem brain tissue showed mitochondrial tRNA levels dropped as Parkinson’s advanced, mirroring CSF trends and highlighting organelle failure as a disease driver.

Blood analysis supported these findings. In postmortem samples, RGTTCRA-tRFs were significantly elevated while MT-tRFs were reduced. Early-stage, mutation-carrying patients displayed a higher RGTTCRA/MT-tRF ratio than healthy carriers of the same mutation. This pattern was consistent across ethnic backgrounds, though slightly less distinct in Black participants, paralleling trends in their clinical scores. Importantly, the GBM model using the tRF ratio achieved a diagnostic accuracy (area under the curve (AUC)) of 0.86, outperforming traditional clinical scores (AUC 0.73). The tRF signature also distinguished prodromal patients, those with early, non-motor symptoms, from healthy controls.

Dual qPCR tests confirmed that this ratio could reliably segregate patients from controls in both fresh blood and postmortem brain samples. Further, RGTTCRA-tRF levels decreased after deep brain stimulation (DBS) treatment, aligning with clinical symptom relief. Patients treated with DBS showed reduced RGTTCRA-tRFs and decreased expression of angiogenin (ANG), indicating that DBS may suppress tRF production or alter their regulation.

Biological analyses provided insight into the potential pathogenic role of RGTTCRA-tRFs. These fragments showed strong sequence complementarity to ribosomal RNA and a leucine tRNA-derived fragment essential for protein translation (LeuCAG3′-tRF). Interaction modeling suggested that RGTTCRA-tRFs could bind both, creating a “dual-lock” mechanism that impairs translation initiation and elongation. Ribosomal profiling of depolarized neuroblastoma cells revealed reduced association of RGTTCRA-tRFs with ribosomes, supporting their role in translation disruption. Förster resonance energy transfer (FRET) imaging confirmed close proximity between RGTTCRA-tRFs and ribosomes in live cells.

Conclusions

To summarize, this study presents compelling evidence that transfer RNA fragments (specifically, RGTTCRA-tRFs and MT-tRFs) can serve as early, non-invasive blood-based biomarkers for PD. Their distinct pattern enables accurate diagnosis even in prodromal stages, outperforming traditional clinical scoring. The dual qPCR test is fast, cost-effective, and sensitive, making it highly applicable in clinical settings. Moreover, these tRFs may play a role in disease progression by interfering with protein synthesis. While findings require validation in larger and more diverse cohorts, particularly in underrepresented ethnic groups, this biomarker strategy offers a promising path toward earlier detection, better monitoring, and more effective therapeutic intervention in PD.

Journal reference:

• Madrer, N., Vaknine-Treidel, S., Zorbaz, T. et al. Pre-symptomatic Parkinson’s disease blood test quantifying repetitive sequence motifs in transfer RNA fragments. Nat Aging (2025), DOI: 10.1038/s43587-025-00851-z, https://www.nature.com/articles/s43587-025-00851-z

Retinal Changes Emerge Years Before Parkinson's Disease

With your risk of Parkinsons post stroke, does your doctor have enough functioning brain cells to get this into a testing protocol for all stroke patients? 

Parkinson’s Disease May Have Link to Stroke March 2017 

Do you prefer your doctor incompetence in this NOT KNOWING? OR NOT DOING?

Retinal Changes Emerge Years Before Parkinson's Disease

OCT data may one day contribute to Parkinson's screening

by Judy George, Deputy Managing Editor, MedPage Today August 22, 2023

People with Parkinson's disease had retinal changes that could be seen with optical coherence tomography (OCT) years before diagnosis, cross-sectional data suggested.

Both incident and prevalent Parkinson's disease were associated with reduced ganglion cell-inner plexiform layer (GCIPL) and inner nuclear layer (INL) thicknesses, reported Siegfried Karl Wagner, MSc, MD, of University College London in England, and co-authors.

People with prevalent Parkinson's disease had thinner GCIPL (-2.12 μm, P=8.2 × 10^-5) and INL (-0.99 μm, P=2.1 × 10-⁴) after adjusting for age, sex, ethnicity, hypertension, and diabetes, the researchers wrote in Neurologyopens in a new tab or window.

Incident Parkinson's also was associated with thinner GCIPL (HR 0.62 per standard deviation increase, P=0.002) and thinner INL (HR 0.70, P=0.026).

The study "sets new standards for the role of retinal morphology as potential biomarker in neurodegenerative disease," observed Valeria Koska and Philipp Albrecht, MD, both of Heinrich Heine University Düsseldorf in Germany, in an accompanying editorialopens in a new tab or window.

"It not only corroborates previous studies but also provides new evidence, e.g., a reduced thickness of the inner nuclear layer," Koska and Albrecht wrote. "It fosters our understanding that [Parkinson's] is a systemic disease, which extends beyond dopaminergic neurons and also involves the retina as peripheral part of the central nervous system already at a very early and apparently even presymptomatic stage."

The effect sizes in the study were small and the practical value of using retinal OCT images to identify early Parkinson's with the current protocols and technology in clinical care is limited, the editorialists noted.

"However, with the advent of artificial intelligence, they might prove useful for the development of new multivariable prognostic factors based on combinations of several biomarkers," they pointed out.

In previous studies, retinal OCT has shown promise as a diagnostic aid for mild cognitive impairmentopens in a new tab or window and has been studied as a potential biomarker of presymptomatic Alzheimer'sopens in a new tab or window disease.

Wagner and co-authors evaluated prevalent Parkinson's disease among people in the retrospective AlzEye cohortopens in a new tab or window in England and incident disease in the prospective U.K. Biobankopens in a new tab or window cohort.

In the AlzEye cohort, 700 individuals had prevalent Parkinson's disease and 105,770 people were controls. Mean age was about 66 and 51.7% were women. The U.K. Biobank study included 50,405 participants with a mean age of 56 and 54.7% were women. In this cohort, 53 people developed Parkinson's disease over an average of 7.3 years.

All participants had non-mydriatic macula-centered OCT imaging. In the U.K. Biobank cohort, researchers included only participants who had retinal imaging at their initial assessment visit (baseline). U.K. Biobank participants who self-reported Parkinson's disease at baseline were excluded from the study.

Parkinson's disease was defined by diagnostic codes. People with diagnostic codes for all-cause dementia were excluded.

In the AlzEye group, people with Parkinson's were older and more likely to be male, hypertensive, and have diabetes. In the U.K. Biobank cohort, adjusted survival analysis showed that age and male sex were associated with incident Parkinson's disease.

In the U.K. Biobank group, the association between thinner GCIPL or INL and incident Parkinson's disease persisted even when participants diagnosed with Parkinson's in the first 24 months after retinal imaging were excluded.

The study had several limitations, Wagner and colleagues acknowledged. The AlzEye cohort did not have detailed clinical information about Parkinson's status, and retinal changes could not be related to disease duration or severity. Because Parkinson's disease was identified by diagnostic codes, some cases may have been missed.

Future studies are needed to determine whether the progression of GCIPL atrophy is driven by Parkinson's brain changes or whether INL thinning precedes GCIPL atrophy, the researchers added.

"I continue to be amazed by what we can discover through eye scans," Wagner said in a statement. "While we are not yet ready to predict whether an individual will develop Parkinson's, we hope that this method could soon become a pre-screening tool for people at risk of disease."

• 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

This study was funded by Fight for Sight UK, Medical Research Council, U.K. Research & Innovation, the Basque Health Department, and the Wellcome Trust.

Wagner is funded by the Medical Research Council and the Rank Prize. Co-authors reported numerous grants, awards, and fellowships.

Primary Source

Neurology

Source Reference: opens in a new tab or windowWagner SK, et al "Retinal optical coherence tomography features associated with incident and prevalent Parkinson disease" Neurology 2023; DOI: 10.1212/WNL.0000000000207727.

Secondary Source

Neurology

Source Reference: opens in a new tab or windowKoska V, Albrecht P "Inner retinal thickness changes in prevalent and incident Parkinson disease: A potential biomarker with prognostic value?" Neurology 2023; DOI: 10.1212/WNL.0000000000207780.

 

New Assay Hailed as a Game Changer for Early Parkinson's Dx

 You'll want this test so if found your doctors can implement those Parkinson prevention protocols they have already competently set up. 

Parkinson’s Disease May Have Link to Stroke March 2017 (Your doctor has had 6 years to put together Parkinson's prevention protocols. Was your doctor competent in doing that?)

Is this better than these other Parkinson tests? Why doesn't your doctor know that answer?

• parkinsons test (4 posts to March 2021)

 

New Assay Hailed as a Game Changer for Early Parkinson's Dx

An alpha-synuclein seed amplification assay (αSyn-SAA) accurately identifies people with Parkinson's disease (PD), as well as those at risk for PD and those with early, prodromal symptoms, and provides information on molecular subtypes, new research indicates.

"Identifying an effective biomarker for Parkinson's disease pathology could have profound implications for the way we treat the condition, potentially making it possible to diagnose people earlier, identify the best treatments for different subsets of patients, and speed up clinical trials," the study's co-lead author Andrew Siderowf, MD, of the University of Pennsylvania Perelman School of Medicine, Philadelphia, said in a news release.

"Our findings suggest that the αSyn-SAA technique is highly accurate at detecting the biomarker for Parkinson's disease regardless of the clinical features, making it possible to accurately diagnose the disease in patients at early stages," added co-lead author Luis Concha-Marambio, PhD, director of research and development at Amprion, San Diego, California.

The study was published online April 12 in Lancet Neurology.

"New Era" in Parkinson's

The researchers assessed the usefulness of αSyn-SAA in a cross-sectional analysis of 1123 participants in the Parkinson's Progression Markers Initiative (PPMI) cohort from 33 participating academic neurology outpatient practices in 12 countries.

The cohort included individuals with sporadic PD from LRRK2 or GBA variants, healthy controls, individuals with clinical syndromes prodromal to PD (rapid eye movement sleep behavior disorder [RBD] or hyposmia), and nonmanifesting carriers of LRRK2 and GBA variants. Cerebrospinal fluid (CSF) samples from each participant were analyzed using αSyn-SAA.

Overall, αSyn-SAA differentiated PD from healthy controls with 87.7% sensitivity and 96.3% specificity.

Sensitivity of the assay varied across subgroups based on genetic and clinical features. 

Among genetic PD subgroups, sensitivity was highest for GBA PD (95.9%), followed by sporadic PD (93.3%), and lowest for LRRK2 PD (67.5%).

Among clinical features, hyposmia was the most robust predictor of a positive assay result.

Among all PD cases with hyposmia, the sensitivity of the assay was 97.2%, compared with 63.0% for PD without olfactory dysfunction.

Combining genetic and clinical features, the sensitivity of positive αSyn-SAA in sporadic PD with olfactory deficit was 98.6%, compared with 78.3% in sporadic PD without hyposmia.

Most prodromal participants (86%) with RBD and hyposmia had positive αSyn-SAA results, indicating they had α-synuclein aggregates despite not yet being diagnosed with PD.

Among those recruited based on their loss of smell, 89% (16 of 18 participants) had positive αSyn-SAA results. Similarly, in those with RBD, positive αSyn-SAA results were present in 85% of cases (28 of 33). No other clinical features were associated with a positive αSyn-SAA result.

In participants who carried LRRK2 or GBA variants but had no PD diagnosis or prodromal symptoms (nonmanifesting carriers), 9% (14 of 159) and 7% (11 of 151), respectively, had positive αSyn-SAA results.

To date, this is the largest analysis of α-Syn-SAA for the biochemical diagnosis of PD, the researchers say.

The results show that the assay classifies people with PD with "high sensitivity and specificity, provides information about molecular heterogeneity, and detects prodromal individuals before diagnosis," they write.

"These findings suggest a crucial role for the α-synuclein SAA in therapeutic development, both to identify pathologically defined subgroups of people with Parkinson's disease and to establish biomarker-defined at-risk cohorts," they add.

Amprion has commercialized the assay (SYNTap test), which can be ordered online.

"Seminal Development"

The authors of an accompanying editorial note the study "lays the foundation for a biological diagnosis" of PD.   

"We have entered a new era of biomarker and treatment development for Parkinson's disease. The possibility of detecting a misfolded α-synuclein, the pathological hallmark of Parkinson's disease, by employing an SSA, is a seminal development," write Daniela Berg, MD, PhD, and Christine Klein, MD, with University Hospital Schleswig-Holstein, Germany.

"However, to fully leverage the enormous potential of the α-synuclein seed amplification, the test would have to be performed in blood rather than the CSF, a less invasive approach that has proven to be viable," they add.

"Although the blood-based method needs to be further elaborated for scalability, α-synuclein SAA is a game changer in Parkinson's disease diagnostics, research, and treatment trials," they conclude.

The study was funded by The Michael J. Fox Foundation for Parkinson's Research and a consortium of more than 40 private and philanthropic partners. Siderowf has declared consulting for Merck, Parkinson Study Group, and receiving honoraria from Bial. A full list of author disclosures is available with the original article. Berg and Klein have reported no relevant financial relationships.

Lancet Neurol. Published online April 12, 2023. Abstract, Editorial

 

A Supersmeller Can Detect the Scent of Parkinson’s, Leading to an Experimental Test for the Illness

You'll want your doctor testing this on you to establish a baseline. And then if found deliver the Parkinson's prevention protocols your doctor should already have if competent.

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

A Supersmeller Can Detect the Scent of Parkinson’s, Leading to an Experimental Test for the Illness

This Scottish woman’s hypersensitive nose picked up a chemical signature of Parkinson’s disease that has been used to develop a skin-swab diagnostic

• By Diana Kwon on October 11, 2022

Joy Milne. Credit: Chris Watt/Alamy Stock Photo

A Scottish woman named Joy Milne made headlines in 2015 for an unusual talent: her ability to sniff out people afflicted with Parkinson’s disease, a progressive neurodegenerative illness that is estimated to affect nearly a million people in the U.S. alone. Since then a group of scientists in the U.K. has been working with Milne to pinpoint the molecules that give Parkinson’s its distinct olfactory signature. The team has now zeroed in on a set of molecules specific to the disease—and has created a simple skin-swab-based test to detect them.

Milne, a 72-year-old retired nurse from Perth, Scotland, has hereditary hyperosmia, a condition that endows people with a hypersensitivity to smell. She discovered that she could sense Parkinson’s with her nose after noticing her late husband, Les, was emitting a musky odor that she had not detected before. Eventually, she linked this change in scent to Parkinson’s when he was diagnosed with the disease many years later. Les passed away in 2015.

In 2012 Milne met Tilo Kunath, a neuroscientist at the University of Edinburgh in Scotland, at an event organized by the research and support charity Parkinson’s UK. Although skeptical at first, Kunath and his colleagues decided to put Milne’s claims to the test. They gave her 12 T-shirts, six from people with Parkinson’s and six from healthy individuals. She correctly identified the disease in all six cases—and the one T-shirt from a healthy person she categorized as having Parkinson’s belonged to someone who went on to be diagnosed with the disease less than a year later.

Subsequently, Kunath, along with chemist Perdita Barran of the University of Manchester in England and her colleagues, has been searching for the molecules responsible for the change in smell that Milne can detect. The researchers used mass spectrometry to identify types and quantities of molecules in a sample of sebum, an oily substance found on the skin’s surface. They discovered changes to fatty molecules known as lipids in people with Parkinson’s.

In their latest study, published on September 7 in the American Chemical Society journal JACS Au, the researchers revealed the results of using a simple skin-swab-based test to detect the lipid signature that is indicative of Parkinson’s. By comparing sebum samples from 79 people with Parkinson’s and 71 people without the illness, the team zeroed in on a set of large lipids that could be detected in a matter of minutes using a special type of mass spectrometry in which substances are rapidly transferred from a swab to an analyzer using just a piece of paper.

“I think it’s a very promising set of biomarkers,” says Blaine Roberts, a biochemist at Emory University, who wasn’t involved in the work. He adds that one of the big open questions that remains is how exacting this test can be. While the authors of the September 7 study reported the detailed chemical profile of the unique Parkinson’s signature, they did not include an assessment of its accuracy. According to Barran, based on not-yet-published data, their test appears to be able to determine whether an individual has Parkinson’s with more than 90 percent accuracy.

Tiago Outeiro, a neuroscientist at the University of Göttingen in Germany, who was not involved with the research, says the sebum-based swab test is novel and has clear advantages, such as the ease of sample collection. Outeiro wonders whether people with diseases that share symptoms and pathologies with Parkinson’s disease, such as multiple system atrophy, also have similar chemical markers.

The team is now working with local hospitals to determine whether this sebum-based test can also be conducted in clinical labs—a key step toward determining whether it can be used as a diagnostic tool. Ultimately, Barran says, the hope is to use the test to help identify individuals who have been referred to their neurologists by their general practitioner for suspected Parkinson’s so they can receive a faster diagnosis. Currently, there are thousands of people waiting to see a neurologist in the U.K.’s National Health Service, and it will take an estimated two years to clear that list, Barran says. A skin-swab test could enable those patients to mail in skin swabs to be analyzed in the hospital laboratory and pinpoint those who need help most urgently. Barran’s research team is approaching people on the waiting list to see if they are willing to take part in a trial to see whether such skin-swab tests could prove effective in helping to speed up the triage process.

Barran and her colleagues are also collaborating with a group at Harvard University to determine whether sebum-based biomarkers are detectable in people who have constipation, a reduced sense of smell or other early signs of Parkinson’s but have not yet received a diagnosis.

Milne has inspired groups elsewhere to search for biomarkers based on the disease’s olfactory signature. This year researchers in China published a paper describing an electronic nose—an artificial-intelligence-based sensor modeled after the olfactory system—that sniffs out molecules present in the sebum of patients with Parkinson’s disease. Other groups in China, the U.K. and elsewhere have also been training dogs to sniff out the disease.

Parkinson’s may not be the only disease Milne has a nose for. She’s also reported noticing a unique smell in people with Alzheimer’s, cancer, and tuberculosis and is working with scientists to see whether a specific olfactory signature of those diseases can be deduced.

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For Milne, the hope is that this work will ultimately benefit patients with these conditions. “My husband suffered from [Parkinson’s] for 21 years after his diagnosis, but he had it many years before that,” Milne told Scientific American in 2015. “I would like to see that people don’t suffer the way he suffered.”

Artificial intelligence model detects Parkinson’s disease via nocturnal breathing signals

 You'll want your doctor to test for this because of your risk of Parkinsons post stroke. And then implement those Parkinson prevention protocols your doctor won't have.

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Artificial intelligence model detects Parkinson’s disease via nocturnal breathing signals

An at-home, artificial intelligence-based system identified individuals with Parkinson’s disease and predicted disease severity and progression using nocturnal breathing signals, according to a study in Nature Medicine.

“A relationship between Parkinson’s and breathing was noted as early as 1817, in the work of Dr. James Parkinson,” Dina Katabi, PhD, principal investigator at the MIT Jameel Clinic, said in a related MIT press release. “This motivated us to consider the potential of detecting the disease from one’s breathing without looking at movements.

Source: Adobe Stock.

“Some medical studies have shown that respiratory symptoms manifest years before motor symptoms, meaning that breathing attributes could be promising for risk assessment prior to Parkinson’s diagnosis.”

Katabi and colleagues evaluated the AI model using a dataset of 7,671 individuals from several sources, including the Mayo Clinic, Massachusetts General Hospital sleep lab and observational clinical trials. The dataset contained 11,964 nights of more than 120,000 hours of nocturnal breathing signals from 757 PD patients (mean age, 69.1 years; 27% women) and 6,914 controls (mean age, 66.2 years; 30% women).

Researchers divided data into breathing belt datasets, from polysomnography sleep studies that use a breathing belt for recordings throughout the night, and wireless datasets, which detect nocturnal breathing using a contactless radio device that extracts “breathing from radio waves that bounce off a person’s body during sleep.”

According to study results, nights measured with a breathing belt achieved an area under the curve (AUC) of 0.889 with a sensitivity of 80.22% (95% CI, 70.28-87.55) and specificity of 78.62% (95% CI, 77.59-79.61). With the wireless signal, researchers reported an AUC of 0.906 with a sensitivity of 86.23% (95% CI, 84.08-88.13) and specificity of 82.83% (95% CI, 79.94-85.40).

Researchers also reported that the AI model could predict PD severity and progression based on the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (R = 0.94).

“Our study demonstrates the feasibility of objective, noninvasive, at-home assessment of PD and also provides initial evidence that this AI model may be useful for risk assessment before clinical diagnosis,” the authors wrote.

According to Katabi, these study findings have important implications for PD treatment and care. “In terms of drug development, the results can enable clinical trials with a significantly shorter duration and fewer participants, ultimately accelerating the development of new therapies,” Katabi said in the release. “In terms of clinical care, the approach can help in the assessment of Parkinson’s patients in traditionally underserved communities, including those who live in rural areas and those with difficulty leaving home due to limited mobility or cognitive impairment.”

Reference:

Artificial intelligence model can detect Parkinson’s from breathing patterns. https://news.mit.edu/2022/artificial-intelligence-can-detect-parkinsons-from-breathing-patterns-0822. Published Aug. 22, 2022. Accessed Aug. 25, 2022.

An Early Sign of Parkinson’s Disease

Not going to help me, I gave up handwriting in college, couldn't read my notes afterwards.

With your heightened chance of getting Parkinsons due to your stroke, your doctor should have this test in their protocol. So if positive they can initiate the Parkinsons prevention protocols. I don't give a damn that those prevention protocols don't exist yet. Your doctor and hospital ARE RESPONSIBLE FOR GETTING THEM CREATED, only four years of incompetence in not getting them created. Or you can let sleeping dogs lie and let them be incompetent in peace. What other business allows failure to continue for decades at a time? Obviously failure is an option in the medical world because the failures don't impact the providers directly.

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

An Early Sign of Parkinson’s Disease

Parkinson’s is a neurological condition caused by loss of brain cells in a critical area of the brain.

Small changes to handwriting can be the first sign of Parkinson’s disease, research finds.

People with Parkinson’s often notice their handwriting becoming smaller and more cramped together.

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It may also be more difficult to write for longer periods of time.

The changes are caused by the onset of muscle stiffness in the hands and fingers caused by Parkinson’s.

Other symptoms of Parkinson’s include stiff limbs and problems standing or walking.

The conclusions come from a study of 40 adults, half of whom were known to be in the first stages of Parkinson’s disease.

They were asked to write their names and copy some addresses.

Computer analysis of their handwriting was able to determine with 97.5% accuracy who had a Parkinson’s diagnosis.

Along with smaller writing and pressing down more softly, people with Parkinson’s spent longer with their pen in the air.

Professor Sara Rosenblum, the study’s first author, explained:

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“This finding is particularly important because while the patient holds the pen in the air, his mind is planning his next action in the writing process, and the need for more time reflects the subject’s reduced cognitive ability.

Changes in handwriting can occur years before a clinical diagnosis and therefore can be an early signal of the approaching disease.”

Professor Rosenblum continued:

“Identifying the changes in handwriting could lead to an early diagnosis of the illness and neurological intervention at a critical moment.”

 

CSF Biomarker Flags Parkinson's Pathology Years Before Symptoms Appear

 With your heightened chance of getting Parkinsons due to your stroke, your doctor should have this test in their protocol. So if positive they can initiate the Parkinsons prevention protocols. I don't give a damn that those prevention protocols don't exist yet. Your doctor and hospital ARE RESPONSIBLE FOR GETTING THEM CREATED, only three years to get them created. Or you can let sleeping dogs lie and let them be incompetent in peace. What other business allows failure to continue for decades at a time? Obviously failure is an option in the medical world because the failures don't impact the providers directly.

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

CSF Biomarker Flags Parkinson's Pathology Years Before Symptoms Appear

Strong sensitivity, specificity in early study

by Judy George, Senior Staff Writer, MedPage Today March 4, 2021

Real-time quaking-induced conversion (RT-QuIC), a test for pathological misfolded protein, detected alpha-synuclein in the cerebrospinal fluid (CSF) of patients with isolated rapid-eye-movement (REM) sleep behavior disorder (IRBD), years before clinical symptoms of Parkinson's disease or dementia with Lewy bodies emerged.

In these patients, RT-QuIC detected misfolded alpha-synuclein in CSF with both sensitivity and specificity of 90%, reported Alison Green, PhD, of the University of Edinburgh in Scotland, and co-authors, in Lancet Neurology. Alpha-synuclein positivity was associated with increased risk of subsequent diagnosis of Parkinson's disease or dementia with Lewy bodies.

"The detection of pathological alpha-synuclein preceded the development of clinical symptoms by a mean of 3.2 years, with a range of 6 months to 9 years," Green said.

"This is the first step towards having a reliable biomarker for early, pre-symptomatic disease which will enable therapeutic interventions, including potential neuroprotective treatments,(What the fuck are those treatments? Useless since you didn't point to where those treatments are listed.) to start in a more timely manner," she told MedPage Today.

RT-QuIC was developed initially to detect abnormally folded prion protein. The "technique is based on prion seed-induced misfolding and aggregation of recombinant protein substrate, accelerated by alternating cycles of shaking and rest in fluorescence plate readers," said Inga Zerr, MD, of the Georg-August University in Göttingen, Germany, in an accompanying editorial.

Seeding activity of misfolded alpha-synuclein had previously been studied in people with Parkinson's disease and dementia with Lewy bodies using brain tissue, CSF, submandibular gland tissues, olfactory mucosa samples, and skin biopsies, Zerr added.

IRBD can be part of the prodromal stage of Parkinson's disease and dementia with Lewy bodies. In this study, Green and colleagues evaluated CSF samples obtained from 52 patients who had IRBD confirmed by video polysomnography at a sleep disorders center in Barcelona and 40 matched controls who were free of neurological disease.

Lumbar punctures for CSF were obtained from 2008 to 2017. Mean follow-up from lumbar puncture until the end of the study in 2020 was 7.1 years in the IRBD group and 7.7 years in controls.

During follow-up, 32 patients (62%) were diagnosed with Parkinson's disease or dementia with Lewy bodies a mean 3.4 years after lumbar puncture, of whom 31 (97%) were alpha-synuclein positive at baseline. Specifically, 16 people developed Parkinson's (15 of whom were positive for CSF alpha-synuclein), and 16 developed dementia with Lewy bodies (all were positive for CSF alpha-synuclein).

CSF alpha-­synuclein RT-­QuIC was positive in 47 (90%) of 52 patients and in four (10%) of 40 healthy controls, resulting in a sensitivity of 90.4% (95% CI 79.4–95.8) and a specificity of 90.0% (95% CI 76.9–96.0).

The average interval for people who were alpha-synuclein positive at baseline to convert to clinically defined Parkinson's or dementia with Lewy bodies was 3.2 years. Patients with IRBD who were alpha-synuclein negative had lower risk for developing Parkinson's disease or dementia with Lewy bodies at 2, 4, 6, 8, and 10 years of follow-up than patients with IRBD who were alpha-synuclein positive. During follow-up, none of the controls developed an alpha-synucleinopathy.

"This result clearly demonstrates the potential of the RT-QuIC method to detect alpha-synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, early before typical clinical manifestation," Zerr said.

"However, a matter that needs to be addressed further in longitudinal studies is the interpretation of positive test results in a cross-sectional setting," she continued. "There were four positive test reactions in 40 healthy controls and in 16 patients with IRBD who did not (by the end of the study) develop clinical symptoms indicative of alpha-synucleinopathy. The probability of some participants having a subclinical alpha-synucleinopathy that did not evolve into Parkinson's disease or dementia with Lewy bodies within the observation period cannot be excluded and requires further investigation."

Other limitations, Green and co-authors noted, were that the results are based on a single­-center study with a fairly small number of participants.

• 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 Department of Health and Social Care Policy Research Programme, the Scottish Government, and the Weston Brain Institute.

Green reported no competing interests; co-authors reported relationships with AbbVie, Roche, Takeda, Jazz, UCB, Wave Pharmaceuticals, Teva, Bial, Prevail, Boehringer Ingelheim, Biogen, the Spanish Network for Research on Neurodegenerative Disorders, and the Michael J. Fox Foundation for Parkinson's Research.

Zerr reported no conflicting interests.

Primary Source

Lancet Neurology

Source Reference: Iranzo A, et al "Detection of α-synuclein in CSF by RT-QuIC in patients with isolated rapid-eye-movement sleep behaviour disorder: a longitudinal observational study" Lancet Neurology 2021; DOI: https://doi.org/10.1016/S1474-4422(20)30449-X.

Secondary Source

Lancet Neurology

Source Reference: Zerr I "RT-QuIC for detection of prodromal α-synucleinopathies" Lancet Neurology 2021; DOI: https://doi.org/10.1016/S1474-4422(21)00036-3.