New Tool Predicts Dementia Years Before Onset

 

 With your excellent chance of getting dementia post stroke what are the EXACT DEMENTIA PREVENTION PROTOCOLS from your doctor?

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 

Maybe because s/he has nothing in the way of a dementia prevention protocol?  There is no excuse for such incompetency, see the following; You are on your own for prevention.

• dementia prevention (261 posts to November 2015)
• Alzheimers prevention (141 posts to November 2021)

New Tool Predicts Dementia Years Before Onset

A new predictive tool combining amyloid PET data with key clinical factors estimates an individual’s lifetime risk for mild cognitive impairment (MCI) and dementia years before symptoms, potentially transforming the way risk is assessed.

The model combines age, sex, APOE-ε4 status and findings on amyloid PET scans, with amyloid PET results having the largest effect on risk. The lifetime and 10-year absolute risk for MCI and dementia in older adults with normal cognition increased continuously with increasing centiloid value for all combinations of sex and APOE-ε4 status.

“This tool will allow patients to determine their likelihood of developing cognitive impairment in the near future when trying to decide if they should consider therapy. This will be necessary if and when therapies become approved for treating cognitively normal persons who are amyloid-positive,” study investigator Ronald Petersen, MD, PhD, neurologist and director of the Mayo Clinic Study of Aging, told Medscape Medical News.

The study was published online on November 12 in Lancet Neurology.

Flagging Early-Intervention Candidates

The lifetime risk of developing cognitive impairment among individuals who are cognitively normal but have abnormal Alzheimer’s disease (AD) biomarkers remains a key knowledge gap.Using data from the long-running Mayo Clinic Study of Aging, Petersen and colleagues developed a prediction model to gauge lifetime and 10-year absolute risk for cognitive impairment in adults aged 50 or older at enrollment.

The primary predictor of interest was biological AD severity, based on amyloid PET centiloid value. Other predictors were starting age, sex, and APOE-ε4 status. Analyses were based on 5158 adults (51% women) who were cognitively unimpaired and 700 individuals (44% women) with MCI.

The researchers observed that an individual’s lifetime risk for MCI and dementia increased uniformly with increasing amyloid PET centiloid value (P < .0001), which was the predictor with the largest effect.

Lifetime risk for MCI for male APOE-ε4 carriers who were cognitively unimpaired at age 75 years was 56.2% for centiloid 5, 60.2% for centiloid 25, 71.0% for centiloid 50, 75.2% for centiloid 75, and 76.5% for centiloid 100.

For female APOE-ε4 carriers who were cognitively normal at age 75 years, lifetime risk for MCI was 68.9% for centiloid 5, 71.3% for centiloid 25, 77.6% for centiloid 50, 81.2% for centiloid 75, and 83.8% for centiloid 100.

“The high lifetime risk in participants with higher centiloid values addresses academic controversies concerning risk of future impairment associated with biomarkers of Alzheimer’s disease among individuals who are cognitively unimpaired,” the authors noted.

Within each centiloid group, lifetime and 10-year absolute risk for MCI and dementia was greater for APOE-ε4 carriers than for noncarriers (P < .0001), “consistent with previous evidence that APOE-ε4 confers deleterious effects beyond those measured by amyloid PET severity,” they noted.

“We anticipate that lifetime and 10-year absolute risk estimates from amyloid PET (or plasma surrogates) will be important for clinicians in the future when weighing the risks vs benefits of therapeutic interventions in patients who are cognitively unimpaired,” they concluded.

A Step Toward Dementia Prevention

Reached for comment, Christopher Weber, PhD, Alzheimer’s Association senior director of global science initiatives, said a “unique aspect” of the study is that it looked at lifetime risk rather than relative risk.

“Relative risk is helpful in research where you’re comparing two groups, for example, high vs low amyloid burden, and determining their chances of developing Alzheimer’s disease. But absolute or lifetime risk answers a question people really care about: What’s my risk, or what are my chances?” Weber told Medscape Medical News.

The observation that lifetime and absolute risk for MCI and dementia were most closely related to increasing biological severity of AD “supports recent and ongoing efforts, led by the Alzheimer’s Association, to define the diagnosis and staging of the disease by its biology,” Weber said.

He cautioned that this is “not a diagnostic tool,” but from an intervention or treatment standpoint, these data are “exciting, if replicated and confirmed, in how they could help patients, families, and their doctors discuss and decide what interventions may be appropriate at the very early stages of this disease.”

Weber said it’s also important to note that the study population was 98% White, relatively healthy, and well-educated. “This limits our ability to generalize the study findings and applicability of this tool to other individuals and populations. It strengthens the call for replication in more representative study populations,” he said.

The authors of a linked commentary noted that the field of dementia is “decisively” moving towards prevention programs for MCI and dementia, following the successful model of the vascular prevention of stroke, myocardial infarction, and peripheral artery disease.

“In such programs, the assessment of amyloid-related risk for neurodegeneration will take place in the context of a comprehensive assessment of all other known risk factors for MCI and dementia,” wrote Giovanni Frisoni, MD, and Augusto Mendes, PhD, with University of Geneva, Geneva, Switzerland.

“The shared vision is that risk profiling will be followed by personalized, domain-specific risk-reduction interventions with nonpharmacological and pharmacological strategies such as monoclonal antibodies, which are actively being developed,” Frisoni and Mendes added.

Funding for the study was provided by the US National Institutes of Health, GHR Foundation, and Alexander Family. Petersen declared having consulted for Roche, Genentech, Eli Lilly, Nestle, and Eisai; participating on a data safety monitoring board for Genentech; and receiving royalties from UpToDate and Oxford University Press for Mild Cognitive Impairment. Frisoni declared receiving fees for consulting from Biogen, Diadem, Eisai, Lilly, Roche, and Synaptica and fees for lectures, presentations, speakers bureaus, manuscript writing, or educational events from Biogen, Roche, Novo Nordisk, and GE HealthCare. Mendes had no disclosures.