Pre-bomb marine reservoir variability in the Kimberley region, Western Australia

New ΔR values are presented for 10 known-age shells from the Kimberley region of northwest Australia. Previous estimates of ΔR for the Kimberley region are based on only 6 individual shell specimens with dates of live collection known only to within 50 yr (Bowman 1985a). Here, we describe the results of our recent attempts to constrain ΔR variability for this region by dating a suite of known-age pre-AD 1950 shell samples from the Australian Museum and Museum Victoria. A regional ΔR of 58 ± 17 14C yr for open waters between Broome and Cape Leveque is recommended based on 7 of these specimens. The criteria used to select shells for dating and inclusion in the regional mean are discussed.Copyright Information: http://www.sherpa.ac.uk/romeo/issn/0033-8222

Learning to be inflexible: Enhanced attentional biases in Parkinson\u27s disease

Impaired attentional flexibility is considered to be one of the core cognitive deficits in Parkinson\u27s disease (PD). However, the mechanisms that underlie this impairment are contested. Progress in resolving this dispute has also been hindered by the fact that cognitive deficits in PD are heterogeneous; therefore, it is unclear whether attentional impairments are only present in a subgroup of patients. Here, we demonstrate that what differentiates PD patients from age-matched controls is an inability to shift attention away from previously relevant information (perseveration) and an inability to shift attention towards previously irrelevant information (learned irrelevance). In contrast, there was no evidence that PD patients, compared to controls, were impaired in being able to appropriately attend to, or ignore, novel information. Furthermore, when patients were stratified according to their level of executive impairment, the executively impaired group showed a selective deficit in set formation compared to the unimpaired group, a behavioural pattern reminiscent of cortical dopamine depletion. Cumulatively, these results suggest that cognitive inflexibility in PD relates to a specific form of attentional dysfunction, in which learned attentional biases cannot be overcome

Spatial structure normalises working memory performance in Parkinson\u27s disease

Cognitive deficits are a frequent symptom of Parkinson\u27s disease (PD), particularly in the domain of spatial working memory (WM). Despite numerous demonstrations of aberrant WM in patients, there is a lack of understanding about how, if at all, their WM is fundamentally altered. Most notably, it is unclear whether span – the yardstick upon which most WM models are built – is compromised by the disease. Moreover, it is also unknown whether WM deficits occur in all patients or only exist in a sub-group who are executively impaired. We assessed the factors that influenced spatial span in medicated patients by varying the complexity of to-be-remembered items. Principally, we manipulated the ease with which items could enter – or be blocked from – WM by varying the level of structure in memoranda. Despite having similar levels of executive performance to controls, PD patients were only impaired when remembering information that lacked spatial, easy-to-chunk, structure. Patients\u27 executive function, however, did not influence this effect. The ease with which patients could control WM was further examined by presenting irrelevant information during encoding, varying the level of structure in irrelevant information and manipulating the amount of switching between relevant and irrelevant information. Disease did not significantly alter the effect of these manipulations. Rather, patients\u27 executive performance constrained the detrimental effect of irrelevant information on WM. Thus, PD patients\u27 spatial span is predominantly determined by level of structure in to-be-remembered information, whereas their level of executive function may mitigate against the detrimental effect of irrelevant information

Dopamine D2 receptor stimulation modulates the balance between ignoring and updating according to baseline working memory ability

BACKGROUND:Working memory (WM) deficits in neuropsychiatric disorders have often been attributed to altered dopaminergic signalling. Specifically, D2 receptor stimulation is thought to affect the ease with which items can be gated into and out of WM. In addition, this effect has been hypothesised to vary according to baseline WM ability, a putative index of dopamine synthesis levels. Moreover, whether D2 stimulation affects WM vicariously through modulating relatively WM-free cognitive control processes has not been explored. AIMS:We examined the effect of administering a dopamine agonist on the ability to ignore or update information in WM. METHOD:A single dose of cabergoline (1 mg) was administered to healthy older adult humans in a within-subject, double-blind, placebo-controlled study. In addition, we obtained measures of baseline WM ability and relatively WM-free cognitive control (overcoming response conflict). RESULTS:Consistent with predictions, baseline WM ability significantly modulated the effect that drug administration had on the proficiency of ignoring and updating. High-WM individuals were relatively better at ignoring compared to updating after drug administration. Whereas the opposite occurred in low-WM individuals. Although the ability to overcome response conflict was not affected by cabergoline, a negative relationship between the effect the drug had on response conflict performance and ignoring was observed. Thus, both response conflict and ignoring are coupled to dopaminergic stimulation levels. CONCLUSIONS:Cumulatively, these results provide evidence that dopamine affects subcomponents of cognitive control in a diverse, antagonistic fashion and that the direction of these effects is dependent upon baseline WM

Caffeine and attentional control:improved and impaired performance in healthy older adults and Parkinson’s disease according to task demands

INTRODUCTION: Caffeine is frequently consumed to boost goal-directed attention. These procognitive effects may occur due to the adenosine-mediated enhancement of monoamines, such as dopamine, after caffeine administration. As such, caffeine’s beneficial effects may be altered in conditions such as Parkinson’s disease (PD). However, whether caffeine improves cognition, and at what cost, has not been experimentally established in patients with neurodegenerative disease. METHODS: Single-dose trials to probe cognitive effects of caffeine are often confounded by short-term caffeine abstinence which conflates caffeine’s effects with treatment of withdrawal. Using a placebo controlled, blinded, randomised trial design, we assessed the effect of 100 mg of caffeine across well-established tasks (Choice reaction time, Stroop Task and Rapid Serial Visual Presentation Task; RSVP) that probe different aspects of attention in PD patients (n = 24) and controls (n = 44). Critically, participants withdrew from caffeine for a week prior to testing to eliminate the possibility that withdrawal reversal explained any cognitive benefit. RESULTS: Caffeine administration was found to reduce the overall number of errors in patients and controls on the Stroop (p = .018, η(2)(p) = .086) and Choice reaction time (p < . 0001, η(2)(p) = .588) tasks, but there was no specific effect of caffeine on ignoring irrelevant information in the Stroop task. On the RSVP task, caffeine improved dual item accuracy (p = .037) but impaired single item accuracy (p = .044). Across all tasks, there was little evidence that caffeine has different effects in PD participants and controls. CONCLUSION: When removing withdrawal effects as a factor, we demonstrate caffeine has beneficial effects on selective attention but is a double-edge sword for visual temporal attention and would need careful targeting to be clinically useful. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00213-021-06054-9

Self-reported intake of high-fat and high-sugar diet is not associated with cognitive stability and flexibility in healthy men

Animal studies indicate that a high-fat/high-sugar diet (HFS) can change dopamine signal transmission in the brain, which could promote maladaptive behavior and decision-making. Such diet-induced changes may also explain observed alterations in the dopamine system in human obesity. Genetic variants that modulate dopamine transmission have been proposed to render some individuals more prone to potential effects of HFS. The objective of this study was to investigate the association of HFS with dopamine-dependent cognition in humans and how genetic variations might modulate this potential association. Using a questionnaire assessing the self -reported consumption of high-fat/high-sugar foods, we investigated the association with diet by recruiting healthy young men that fall into the lower or upper end of that questionnaire (low fat/sugar group: LFS, n = 45; high fat/sugar group: HFS, n = 41) and explored the interaction of fat and sugar consumption with COMT Va1158Met and Taq1A genotype. During functional magnetic resonance imaging (fMRI) scanning, male partici-pants performed a working memory (WM) task that probes distractor-resistance and updating of WM repre-sentations. Logistic and linear regression models revealed no significant difference in WM performance between the two diet groups, nor an interaction with COMT Va1t58Met or Tag1A genotype. Neural activation in task -related brain areas also did not differ between diet groups. Independent of diet group, higher BMI was associ-ated with lower overall accuracy on the WM task. This cross-sectional study does not provide evidence for diet -related differences in WM stability and flexibility in men, nor for a predisposition of COMT Va1158Met or Tag1A genotype to the hypothesized detrimental effects of an HFS diet. Previously reported associations of BMI with WM seem to be independent of HFS intake in our male study sample.Peer reviewe

Dopamine affects short-term memory corruption over time in Parkinson’s disease

Cognitive deficits are a recognised component of Parkinson’s disease (PD). However, particularly within the domain of short-term memory, it is unclear whether these impairments are masked, or caused, by patients’ dopaminergic medication. The effect of medication on pure maintenance in PD patients has rarely been explored, with most assessments examining maintenance intercalated between other executive tasks. Moreover, few studies have utilised methods that can measure the quality of mental representations, which can enable the decomposition of recall errors into their underlying neurocognitive components. Here, we fill this gap by examining pure maintenance in PD patients in high and low dopaminergic states. Participants had to encode the orientation of two stimuli and reproduce these orientations after a short (2 s) or long (8 s) delay. In addition, we also examined the performance of healthy, age-matched older adults to contextualise these effects and determine whether PD represents an exacerbation of the normal ageing process. Patients showed improved recall OFF compared to ON their dopaminergic medication, but only for long-duration trials. Moreover, PD patients OFF their medication actually performed at a level superior to age-matched controls, indicative of a paradoxical enhancement of memory in the low dopaminergic state. The application of a probabilistic model of response selection suggested that PD patients made fewer misbinding errors in the low, compared with high, dopaminergic state for longer-delay trials. Thus, unexpectedly, the mechanisms that prevent memoranda from being corrupted by misbinding over time appear to be enhanced in PD patients OFF dopaminergic medication. Possible explanations for this paradoxical effect are discussed

Effects of cholinesterase inhibition on attention and working memory in Lewy body dementias

Cholinesterase inhibitors are frequently used to treat cognitive symptoms in Lewy body dementias (Parkinson’s disease dementia and Dementia with Lewy bodies). However, the selectivity of their effects remains unclear. In a novel rivastigmine-withdrawal design, Parkinson’s disease dementia and Dementia with Lewy bodies patients were tested twice: once when taking rivastigmine as usual and once when they had missed one dose. In each session, they performed a suite of tasks (sustained attention, simple short-term recall, distractor resistance and manipulating the focus of attention) which allowed us to investigate the cognitive mechanisms through which rivastigmine affects attentional control. Consistent with previous literature, rivastigmine withdrawal significantly impaired attentional efficacy (quicker response latencies without a change in accuracy). However, it had no effects on cognitive control as assessed by the ability to withhold a response (inhibitory control). Worse short-term memory performance was also observed when patients were OFF rivastigmine, but these effects were delay and load-independent, likely due to impaired visual attention. In contrast to previous studies that have examined the effects of dopamine withdrawal, cognitively complex tasks requiring control over the contents of working memory (ignoring, updating or shifting the focus of attention) were not significantly impaired by rivastigmine withdrawal. Cumulatively, these data support the conclusion cholinesterase inhibition has relatively specific and circumscribed – rather than global – effects on attention that may also affect performance on simple short-term memory tasks, but not when cognitive control over working memory is required. The results also indicate that withdrawal of a single dose of rivastigmine is sufficient to reveal these impairments, demonstrating that cholinergic withdrawal can be an informative clinical as well as an investigative tool

Task-irrelevant financial losses inhibit the removal of information from working memory

Abstract The receipt of financial rewards or penalties - though task-irrelevant - may exert an obligatory effect on manipulating items in working memory (WM) by constraining a forthcoming shift in attention or reinforcing attentional shifts that have previously occurred. Here, we adjudicate between these two hypotheses by varying – after encoding- the order in which task-irrelevant financial outcomes and cues indicating which items need to be retained in memory are presented (so called retrocues). We employed a “what-is-where” design that allowed for the fractionation of WM recall into separate components: identification, precision and binding (between location and identity). Principally, valence-dependent effects were observed only for precision and binding, but only when outcomes were presented before, rather than after, the retrocue. Specifically, task-irrelevant financial losses presented before the retrocue caused a systematic breakdown in binding (misbinding), whereby the features of cued and non-cued memoranda became confused, i.e., the features that made up relevant memoranda were displaced by those of non-cued (irrelevant) items. A control experiment, in which outcomes but no cues were presented, failed to produce the same effects, indicating that the inclusion of retrocues were necessary for generating this effect. These results show that the receipt of financial penalties – even when uncoupled to performance – can prevent irrelevant information from being effectively pruned from WM. These results illustrate the importance of reward-related processing to controlling the contents of WM