Here are the reasons your doctor needs to test for this on you AND DELIVER THOSE EXACT DEMENTIA PREVENTION PROTOCOLS! Can't do that; your doctor is incompetent! And why hasn't the board of directors had that doctor fired?
Your risk of dementia, has your doctor
told you of this? Your doctor is responsible for preventing this! Is
s/he willing to prevent 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 study reveals 3 distinct paths of early Alzheimer’s progression
An analysis of more than 1,600 participants from the A4 and LEARN studies identified 3 distinct preclinical Alzheimer’s disease trajectories -- stable, slow decline, and rapid decline -- with nearly 70% of amyloid-positive individuals remaining cognitively stable over time.
Biomarkers such as elevated plasma phosphorylated tau 217 (p-tau217), increased tau positron emission tomography (PET) signal, and reduced hippocampal volume predicted faster decline, underscoring the need for healthcare professionals and researchers to incorporate biomarker-driven stratification in prevention trials to better capture disease progression and improve study power.
The findings were published in Alzheimer’s & Dementia.
“Most studies look at the average across participants, which can make it seem like everyone is slowly getting worse at the same rate,” said Michael Donohue, PhD, University of Southern California (USC) Keck School of Medicine, Los Angeles, California. “But we found that this approach masks major differences between people, suggesting that Alzheimer’s disease is more variable than often depicted.”
“These results suggest we may need to rethink how we design clinical trials in preclinical Alzheimer’s disease,” said Runpeng (Tony) Li, PhD, USC Keck School of Medicine. “Many people with Alzheimer’s remain stable over the course of a study, which can make it hard to tell if a treatment is working. Identifying those who are more likely to decline could make trials more efficient and more informative.”
The researchers analysed data from cognitively unimpaired adults enrolled in the Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease (A4) study (amyloid beta-positive participants), and the Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) study (amyloid beta-negative individuals).
Using latent class mixed-effects modeling, they identified distinct cognitive trajectories over time and examined how baseline clinical measures, imaging findings, and blood-based biomarkers were associated with different patterns of decline, with the Preclinical Alzheimer Cognitive Composite serving as the primary outcome measure.
The analysis revealed 3 distinct trajectory classes (stable, slow decline, and paid decline) with striking heterogeneity even among amyloid-positive individuals, approximately 70% of whom remained cognitively stable. Elevated plasma p-tau217, increased tau PET burden, and reduced hippocampal volume were strongly associated with declining classes.
The researchers noted that current trials may be oversimplifying Alzheimer’s disease by assuming everyone follows the same path. In addition, in the disease’s early stages, many participants may remain stable even without treatment, making it harder to detect whether a drug is working. The researchers plan to further examine participants who were predicted to remain stable but worsened, or those predicted to decline who remained symptom-free.
“What is different about certain patients that makes them more resilient -- and can these insights be leveraged to slow down Alzheimer’s disease in others?” Donohue said.
Reference: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.71366
SOURCE: University of Southern California Keck School of Medicine
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