On your own to figure this out for yourself, women were not well represented. My mom at 91 is still going strong. Dad at 91 died with Parkinson's dementia. I'm going to hit at least 100, reading right now; 'Lifespan: Why We Age and Why We Don't Have To'. I will then have spent half my life disabled, stroke at 50.
Brain Health When You're 92
Why some people may be resistant to cognitive decline
Over a mean 14 years, baseline cognition at an average age of 77.6 predicted cognitive status at a mean age of 92 (range 86-100), reported Beth Snitz, PhD, of the University of Pittsburgh, and colleagues.
Predictors of cognitive status among Aβ-positive participants were baseline cognitive test scores and smoking history. The APOE2 allele predicted Aβ status, and baseline pulse pressure predicted longitudinal Aβ increase.
Overall, paid work engagement and life satisfaction predicted less cognitive decline, Snitz and colleagues wrote in Neurology.
"The vast majority of research studies on aging and Alzheimer's disease try to understand which risk factors predict disease and dementia," Snitz said.
"We turned the question on its head and asked: Which factors predict resistance to disease and cognitive impairment in the oldest-old?" she told MedPage Today. "The strategy was to discover specific protective factors which may be different, than simply the absence of known risk factors."
The study aimed to look at two facets of successful cognitive aging: resilience in the presence of Alzheimer's pathology, and resistance to Aβ deposition.
"An important question to consider in studies of resilience is whether good performance in an individual with Aβ positivity reflects resilience to amyloid, or merely an earlier stage of Alzheimer disease process," noted Claudia Kawas, MD, and Maria Corrada, ScM, ScD, both of the University of California Irvine, in an accompanying editorial."The 14-year window of this longitudinal study supports the notion that these individuals may indeed be resilient."
In their study, Snitz and colleagues evaluated 100 elderly people who had participated in the Ginkgo Evaluation of Memory Study (GEMS), a trial that studied the effect of Ginkgo biloba on dementia from 2000 to 2008. Some GEMS participants also took part in an imaging sub-study in 2009; a group of those continued to be followed with serial neuroimaging, clinical, and cognitive evaluations in 2010-2011.
Participants were excluded from enrolling in GEMS if they were under age 75 in 2000-2002; had prevalent dementia; were taking warfarin, 400-IU vitamin E, or medication with high anti-cholinergic load; had a history of bleeding disorders, severe depression, or Parkinson's disease; had abnormal metabolic lab values, liver function tests, vitamin B-12, or platelets; or had disease-related life expectancy of fewer than 5 years.
Mean follow-up time from baseline to last measured Aβ status in the cohort was 12.3 years and to last cognitive evaluation was 14.1 years. In the 84 participants who were cognitively normal in 2009, 26 remained that way during follow-up. Mean age at last cognitive evaluation ranged from 86 to 100. Mortality was 54% since 2011 (enrollment into the follow-up study).
Of 100 participants, 30% had normal cognition at the last assessment. The Raven's Progressive Matrices (PM) test, a measure of pre-morbid cognitive ability and reasoning (OR 1.49, 95% CI 1.20-1.86, P<0.001) and the California Verbal Learning Test, a verbal memory measure (OR 1.07, 95% CI 1.01-1.13, P=0.002) were significant predictors of unimpaired cognition at last follow-up.
At the last imaging evaluation, 34 people (34%) of participants were Aβ-negative. The Aβ-negative group had a higher proportion of APOE2 carriers than the Aβ-positive group (21.9% vs 4.8%, OR 5.5, 95% CI 1.3- 23.0, P=0.01).
Of the 66 people who were Aβ-positive, 14 were cognitively unimpaired. These 14 people were not different in APOE genotype and demographic variables from impaired Aβ-positive participants. Never having smoked (OR 10.84, 95% CI 1.50-78.27, P=0.02), and Raven's PM test (OR 1.33, 95% CI 1.04-1.69; P=0.02) were significant predictors of unimpaired cognition.
Baseline vascular health factors and APOE4 predicted overall Aβ deposition across time. Lower baseline pulse pressure was protective against Aβ increase over time.
Few baseline measures predicted differential cognitive change during follow-up, but those that did included current paid work engagement and life satisfaction. Both were protective against memory decline in the whole cohort.
"Although resilience is an important consideration for successful aging, resistance to Aβ deposition at this advanced age is particularly intriguing," Kawas and Corrada observed.
"There is growing evidence that APOE may have effects independent or downstream to amyloid that are relevant to cognitive preservation," they continued. "Although genetics are not modifiable at the moment, in contrast, pulse pressure may represent a modifiable risk factor and should be an area of intense research."
The study is limited in that it looked predominantly at volunteers who largely were male, white, and well-educated, while most people in their 90s are women, the editorialists noted.
Multiple neuropathological abnormalities are very common at advanced ages, and it's also possible that resilience to Alzheimer's pathology in this study may reflect resistance to other pathologies, including hippocampal sclerosis, microvascular disease, and Lewy bodies, they added.
Disclosures
The study was funded by NIH.
Snitz disclosed no relevant relationships with industry. Co-authors disclosed relevant relationships with Amgen, Cognition Therapeutics, Biogen, and GE Healthcare. A author disclosed being a co-inventor of Pittsburgh Compound B (PiB) that which was used in PET imaging in this study and has a financial interest in this license agreement.
Kawas and Corrada disclosed no relevant relationships with industry.
Snitz disclosed no relevant relationships with industry. Co-authors disclosed relevant relationships with Amgen, Cognition Therapeutics, Biogen, and GE Healthcare. A author disclosed being a co-inventor of Pittsburgh Compound B (PiB) that which was used in PET imaging in this study and has a financial interest in this license agreement.
Kawas and Corrada disclosed no relevant relationships with industry.
Primary Source
Neurology
Secondary Source
Neurology
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