Presentations

Read the latest research from Cogstate scientists and technologies as featured in poster and podium presentations from recent industry conferences.

Age increases rate of Aß and ε4 related memory decline in preclinical Alzheimer’s Disease

Presented at CTAD 2016

Older age, high amyloid (Aβ+) and the apolipoprotein E (APOE) ε4 allele are risk factors for Alzheimer’s disease (AD). However, the extent to which increasing age is related to memory decline in the presence of Aβ+ and ε4 is not understood fully.  We aimed to determine the effect of age, Aβ+ and ε4 on memory decline in a large group of older adults who did not meet clinical criteria for AD dementia.

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Impairment and decline on the Cogstate Brief Battery is related to amyloid and hippocampal volume in very mild dementia

Presented at CTAD 2016

The study followed prospectively changes in cognition and hippocampal volume over 72 months in Aβ- and Aβ+ adults with a CDR score of 0.5.  We proposed that at baseline, Aβ- older adults, CDR 0.5 Aβ+ older adults would show large impairments in memory and working memory, and that this would be accompanied by smaller hippocampal volumes.  The second hypothesis was that CDR 0.5 Aβ+ older adults would show faster decline in memory and working memory over 72-months and that this would also be accompanied by increased loss of hippocampal volume.   The third hypothesis was that any cognitive decline observed in CDR 0.5 Aβ- older adults would be less than that observed in CDR 0.5 Aβ+ older adults.

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Effects of Aβ and BDNF Val66Met on episodic memory, hippocampal volume and serum BDNF in preclinical Alzheimer’s disease

Presented at AAIC 2016

In non-demented older adults carriage of the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism Met allele exacerbates amyloid (Aβ) related decline in episodic memory and hippocampal volume loss over 36 months. The extent to which Aβ+ and BDNF Val66Met is related to circulating markers of BDNF (e.g., serum) is unknown. The aim of this study was to determine the effect of Aβ+ and the BDNF Val66Met polymorphism on levels of serum mature BDNF (mBDNF), episodic memory and hippocampal volume at baseline and over 18-months in non-demented older adults.

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Aβ related memory decline and hippocampal volume loss in very mild dementia

Presented at AAIC 2016

Older adults who report a noticeable decline in cognitive abilities are now investigated for early dementia. If this is corroborated by objective evidence of cognitive impairment, individuals can be considered to be in the early stages of dementia. This early stage of dementia is staged clinically at the 0.5 level on the Clinical Dementia Rating (CDR) scale, and has various terms such as ‘very mild dementia’ or ‘mild cognitive impairment’ (MCI). Recent consensus criteria that integrate risk from biomarkers and the amyloid cascade hypothesis stipulate that individuals with a CDR score of 0.5 and who are also Aβ+ can be considered as having prodromal AD. Such criteria also raises the hypothesis that the pathological processes underlying cognitive impairment in individuals who are CDR 0.5 but who have low levels of cerebral Aβ (Aβ-) may reflect neurodegenerative or psychiatric processes other than AD. However, the nature and magnitude of cognitive decline associated with known biomarkers of AD (i.e., cerebral Aβ, hippocampal volume) in individuals with CDR O.S remain poorly defined. In a group of older adults with very mild dementia, we aimed to characterize the nature and magnitude of cognitive decline as measured by the Cogstate Brief Battery, in relation to AP levels and hippocampal volume. Participants were characterized according to their status on the Clinical Dementia Rating (CDR) scale.

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Plasma cortisol, amyloid-β, and cognitive decline in preclinical Alzheimer’s disease: A 6-year prospective cohort study

Presented at AAIC 2016

Hypothalamic-pituitary-adrenal (HPA) axis dysregulation, which is typically assessed by measuring cortisol levels, is associated with cognitive dysfunction, hippocampal atrophy, and increased risk for mild cognitive impairment and Alzheimer disease (AD). However, little is known about the role of HPA axis dysregulation in predicting cognitive decline or in moderating the effect of high levels of amyloid-β (Aβ+) on cognitive decline in the preclinical phase of AD, which is often protracted, and thus offers opportunities for prevention and early intervention. We aimed to evaluate the independent and interactive effect of plasma cortisol levels and Aβ status in predicting cognitive changes in the preclinical phase of AD.

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