Pat & Dennis Bender Early Dementia Diagnosis & Prognosis Fund
J. Dennis Bender
Office, Home & Cell Phone: 859-391-5226
5726 La Jolla Blvd. – Suite 311
La Jolla, CA 92037-7345
&
Office - 100 Riverside Pl. - Suite 303
Covington, KY 41011-5711
We support the development of improved diagnostic methods for the early detection and diagnosis of MCI, Alzheimer’s, vascular and other dementias, their likely prognosis, and best treatment options. We focus on the development of Bayesian-based medical-decision-support systems, comparative-effectiveness research, and the better utilization of these for the above. (After incorporating in KY as a 501(c)(3) in 2002, we dissolved that entity for a simplified form of two entirely self-financed, private philanthropies utilizing a Vanguard Charitable Trust for making annual-research-grants for early-dementia-detection and its correct differential-diagnosis and likely-prognosis. They will continue on, after I am gone, either mentally or physically. Prof. Randall Bateman is the first of our fund’s research advisors.
See: https://www.alz.org/alzheimers-dementia/research_progress/earlier-diagnosis )
www.JDBender.com – EMS/eVTOL Experimental Aviation Fund (Vanguard Charitable Trust)
www.JDBender.org – Dementia Diagnosis Fund (Vanguard Charitable Trust)
[My favorite image but no credit for it provided in this article so I don’t know where it comes from to credit it.]
“The idea is that could we come up with a peripheral-marker to reflect the underlying-brain-pathology that's easier-to-obtain, faster-to-run, and that we could screen-population-wise. . . This marker-panel could predict-clinical-AD-diagnosis and improved-the-prediction-of-disease-trajectories-for-cognitive-decline-and-dementia compared with Aβ42, pTau181, and tTau alone. Prediction-performance could be further improved by combining the protein-panel and these canonical-biomarkers.”
More on this important topic of improving AD-diagnosis and predictions-of-its-progression using a 48-protein-panel combined with other existing biomarkers, one of my own focus-areas for my research-grant-funding in 2024.
This 48-protein-panel was at least as effective at predicting-clinical-diagnosis and measures-of-cognitive-and-dementia-severity as existing-CSF-biomarkers such as amyloid-beta and tau. Adding the panel to the existing CSF-biomarkers significantly-improved diagnostic-performance across all the studied endpoints. The combined-test was the most-effective way to predict-cognitive-decline and dementia-severity. Simple as that.
Here is another short summary of this potentially very-important new research that I previously reviewed in much-greater-detail. Obviously, it next needs to be extended to a larger, more-diverse, sample and then have this new test procedure standardized, so that it can be run in any State-approved, CLIA-certified lab and cleared for general-use outside just academic-research settings.
Protein-Panel Improves Alzheimer’s-Diagnosis, Predictions of Disease-Progression
Nick Paul Taylor - Oct 3, 2023 – LabPulse.com
Quantifying certain proteins in cerebrospinal-fluid (CSF) could improve-the-diagnosis-of-Alzheimer's-disease and prediction-of-disease-progression, according to a paper in Science Translational Medicine.
The recognition that people with Alzheimer’s undergo biological-changes years-before the onset-of-clinical-symptoms has spurred research into markers that may enable physicians to detect the disease before cognitive decline begins. Bringing forward disease-detection may lead to improved-health-outcomes if it is combined with the development of interventions that are effective in preclinical-patients.
That prospect led researchers at Emory University to use a high-throughput-mass-spectrometry-assay to quantify 48-proteins in CSF-samples. The samples were taken from 706 participants in the Alzheimer's Disease Neuroimaging Initiative; the proteins were selected based on earlier work aimed to integrate CSF and brain-proteome-networks.
Nicholas Seyfried, Professor of Biochemistry at Emory’s School of Medicine and Co-Senior Author with Thomas Wingo and Allan Levey, outlined the thinking behind the approach in a statement.
“The idea is that could we come up with a peripheral-marker to reflect the underlying-brain-pathology that's easier-to-obtain, faster-to-run, and that we could screen-population-wise. Are you higher or lower than the average? You are either in the middle, which means you're normal, or you’re below, which is probably a good thing with this protein-panel. Or you're a standard-deviation above-the-mean. Which would indicate-a-risk-profile,” Seyfried said. [Exactly the thing I am focused on funding!]
The 48-protein-panel was at least as effective at predicting-clinical-diagnosis and measures-of-cognitive-and-dementia-severity as existing-CSF-biomarkers such as amyloid-beta and tau. Adding the panel to the existing CSF-biomarkers significantly-improved diagnostic-performance across all the studied endpoints. The combined-test was the most-effective way to predict-cognitive-decline and dementia-severity.
Further validation is needed, but the study suggests that the 48-protein-panel complements existing CSF-biomarkers and may improve the diagnosis of Alzheimer’s and the prediction of cognitive-decline and severity-of-dementia. The panel may complement the biomarkers because it “reflects a range of altered-biology observed” in Alzheimer’s and related-disorders, the authors wrote.
Keywords: Diseases, Health-Topics, Alzheimer's
Research Article - Alzheimer's-Disease
A Protein Panel in Cerebrospinal-Fluid for Diagnostic and Predictive Assessment of Alzheimer’s-Disease
Rafi Haque Https://Orcid.Org/0000-0003-0489-9167, Caroline M. Watson Https://Orcid.Org/0000-0001-6574-0833, Jiaqi Liu Https://Orcid.Org/0000-0003-3480-3234, E. Kathleen Carter Https://Orcid.Org/0000-0002-5083-0614, [...], And Allan I. Levey Https://Orcid.Org/0000-0002-3153-502x +9 Authors Info & Affiliations
Science Translational Medicine - 6 Sep 2023 - Vol 15, Issue 712 - DOI: 0.1126/scitranslmed.adg4122
Editor’s Summary Fluid-biomarker-discovery for Alzheimer's-Disease (AD) has made rapid progress but markers to predict-disease-progression are still-needed. Here Haque and colleagues employed a validated, high-throughput, mass-spectrometry-assay to quantify-48-proteins in cerebrospinal-fluid samples from 706-participants recruited from the Alzheimer's Disease Neuroimaging Initiative. The marker-panel could predict-clinical-AD-diagnosis and improved-the-prediction-of-disease-trajectories-for-cognitive-decline-and-dementia compared with Aβ42, pTau181, and tTau. Prediction performance could be further improved by combining the protein-panel and these canonical-biomarkers. While further validation is needed, this protein-panel could help to improve-diagnostics and prognostics of AD. —Daniela Neuhofer
Abstract Alzheimer’s-disease (AD) is a neurodegenerative-disease with heterogenous-pathophysiological-changes that develop-years-before-the-onset-of-clinical-symptoms. These preclinical-changes have generated considerable interest in identifying markers for the pathophysiological mechanisms linked to AD and AD-related disorders (ADRD).
On the basis of our prior work integrating cerebrospinal-fluid (CSF) and brain-proteome-networks, we developed a reliable and high-throughput-mass-spectrometry–selected-reaction-monitoring-assay that targets-48-key-proteins-altered-in-CSF.
To test the diagnostic-utility of these proteins and compare them with existing-AD-biomarkers, CSF collected at baseline-visits was assayed from 706-participants recruited from the Alzheimer’s Disease Neuroimaging Initiative. We found that the targeted-CSF-panel-of-48-proteins (CSF-48-panel) performed at least as well as existing AD-CSF-biomarkers (Aβ42, tTau, and pTau181) for predicting clinical-diagnosis, FDG-PET, hippocampal-volume, and measures-of-cognitive-and-dementia-severity. In addition, for each of those outcomes, the CSF-48-panel plus the existing-AD-CSF-biomarkers significantly-improved-diagnostic-performance. Furthermore, the CSF-48-panel plus existing-AD-CSF-biomarkers significantly-improved-predictions for changes in FDG-PET, hippocampal-volume, and measures-of-cognitive-decline-and-dementia-severity compared with either measure alone. A potential reason for these improvements is that the CSF-48-panel reflects a range-of-altered-biology observed in AD/ADRD. In conclusion, we show that the CSF-48-panel complements existing AD-CSF-biomarkers to improve-diagnosis and predict-future-cognitive-decline-and-dementia-severity.
[Keywords and compound-keywords (tags) are highlighted-and-hyphenated in italic-and-bold; place-names, organizations and titles are in bold; media-names put in italic. Instead of underlining, I’ve been experimenting with hyphenating entire phrases – long-tail-keywords. This odd style was being tried to enhance generative-AI processing and ease-of-spotting items-of-interest in my specific website-achieved documents. Now generative-AI and similar have eliminate this time-consuming distraction.]
{Protein Panel for AD Diagnosis}
1