Amyloid imaging and cognitive decline in nondemented oldest‐old: The 90+ Study

Abstract

Background The goal of this study was to examine cross-sectional and longitudinal associations between cognitive performance and beta amyloid (Aβ) load determined by florbetapir F18 positron emission tomography (PET) in non-demented oldest-old. Methods Thirteen non-demented (normal or cognitively impaired non-demented) participants (median age=94.2 years) from The 90+ Study underwent florbetapir-PET scanning within 3 months of baseline neuropsychological testing. Amyloid load was measured with a semiautomated quantitative analysis of average cortical to cerebellar standard uptake values (SUVr) ratio and a visual interpretation (Aβ- or Aβ+). Neuropsychological testing was repeated every 6 months. Results At baseline, SUVr correlated significantly with tests of global cognition and memory. During follow-up (median=1.5 years), the Aβ+ group had steeper declines on most cognitive tests, particularly global cognitive measures. Conclusion This preliminary study suggests that greater amyloid load is associated with poorer cognition and faster cognitive decline in non-demented oldest-old. Amyloid load may identify individuals at increased risk of developing Alzheimer's disease.

The Evolution of Preclinical Alzheimer’s Disease: Implications for Prevention Trials

“…As the field has matured with large sample sizes, there have been increasing reports of significant amyloid-associated deficits in cognitive performance, even amongst the limited range observed in clinically normal older individuals (Li et al, 2014; Lim et al, 2012 [Epub ahead of print]; Sperling et al, 2013) but the cross-sectional effects remain relatively subtle. The most convincing findings, however, stem from Aβ associated decline in longitudinal studies cognition among those who were CN at baseline (Donohue et al, 2014; Doraiswamy et al, 2012; Doraiswamy et al, 2014; Kawas et al, 2013; Lim et al, 2014b; Lim et al, 2012; Mormino et al, 2014a; Mormino et al, 2014b; Resnick et al, 2010; Storandt et al, 2009). The majority of these studies have indicated that episodic memory shows the greatest vulnerability to Aβ-associated cognitive decline, but other domains of cognition including working memory and executive function have also demonstrated Aβ-associated change (Rodrigue et al, 2012).…”

Neuroimaging markers associated with maintenance of optimal memory performance in late-life

“…However, there are more recent studies suggesting that SuperAgers have a lower frequency of the ApoE-4 allele and fewer surrogate markers for AD (Harrison et al, 2012; Rogalski et al, 2013). Furthermore, greater amyloid burden has been associated with cognitive decline in the oldest-old (age 90+) (Kawas et al, 2013; Snitz et al, 2013). Thus, it remains unclear to what extent optimal cognitive aging in late life reflects resilience to AD pathology or absence of AD pathology.…”

Gut Microbiota, a Key Factor Relating Diet and Inflammation with the Progression of Cognitive Impairment in Older People

“…The presence of amyloid-β (Aβ) protein is a definite risk factor, as 60% of old persons with dementia show presence of Aβ after positron emission tomography (PET) scan, and 40% of healthy volunteers of similar age (>90) showed the presence of Aβ. However, this healthy group positive for Aβ lost their cognitive faculties faster than the healthy group with no Aβ signal [6]. Aβ plates have an important role in AD pathogenesis, but the severity of the cognitive impairment holds greater correlation with the burden of neocortical neurofibrillary tangles than with the presence of Aβ plates [7].…”