Anatomy and Neuroscience - Research Publications

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    Rates of age- and amyloid β-associated cortical atrophy in older adults with superior memory performance
    Dang, C ; Yassi, N ; Harrington, KD ; Xia, Y ; Lim, YY ; Ames, D ; Laws, SM ; Hickey, M ; Rainey-Smith, S ; Sohrabi, HR ; Doecke, JD ; Fripp, J ; Salvado, O ; Snyder, PJ ; Weinborn, M ; Villemagne, VL ; Rowe, CC ; Masters, CL ; Maruff, P (WILEY, 2019-12)
    INTRODUCTION: Superior cognitive performance in older adults may reflect underlying resistance to age-associated neurodegeneration. While elevated amyloid β (Aβ) deposition (Aβ+) has been associated with increased cortical atrophy, it remains unknown whether "SuperAgers" may be protected from Aβ-associated neurodegeneration. METHODS: Neuropsychologically defined SuperAgers (n = 172) and cognitively normal for age (n = 172) older adults from the Australian Imaging, Biomarkers and Lifestyle study were case matched. Rates of cortical atrophy over 8 years were examined by SuperAger classification and Aβ status. RESULTS: Of the case-matched SuperAgers and cognitively normal for age older adults, 40.7% and 40.1%, respectively, were Aβ+. Rates of age- and Aβ-associated atrophy did not differ between the groups on any measure. Aβ- individuals displayed the slowest rates of atrophy. DISCUSSION: Maintenance of superior memory in late life does not reflect resistance to age- or Aβ-associated atrophy. However, those individuals who reached old age without cognitive impairment nor elevated Aβ deposition (i.e. Aβ-) displayed reduced rates of cortical atrophy.
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    COMT val158met is not associated with Aβ-amyloid and APOE ε4 related cognitive decline in cognitively normal older adults
    Porter, T ; Burnham, SC ; Milicic, L ; Savage, G ; Maruff, P ; Sohrabi, HR ; Peretti, M ; Lim, YY ; Weinborn, M ; Ames, D ; Masters, CL ; Martins, RN ; Rainey-Smith, S ; Rowe, CC ; Salvado, O ; Groth, D ; Verdile, G ; Villemagne, VL ; Laws, SM (ELSEVIER, 2019-06)
    The non-synonymous single nucleotide polymorphism (SNP), Val158Met within the Catechol-O-methyltransferase (COMT) gene has been associated with altered levels of cognition and memory performance in cognitively normal adults. This study aimed to investigate the independent and interactional effects of COMT Val158Met on cognitive performance. In particular, it was hypothesised that COMT Val158Met would modify the effect of neocortical Aβ-amyloid (Aβ) accumulation and carriage of the apolipoprotein E (APOE) ε4 allele on cognition in preclinical Alzheimer's disease (AD). In 598 cognitively normal older adults with known neocortical Aβ levels, linear mixed modelling revealed no significant independent or interactional associations between COMT Val158Met and cognitive decline. These findings do not support previous associations between COMT Val158Met and cognitive performance and suggest this variant does not influence Aβ-amyloid or APOE ε4 driven cognitive decline in a well characterised cohort of cognitively normal older adults.