Memory consolidation — Mechanisms and opportunities for enhancement

Abstract Memory consolidation is the process by which relevant information is selected and transferred from a short-term, fragile state, into a stable, longer term domain from which it can be recalled. Effective memory underpins our ability to carry out everyday activities. When memory consolidation fails, such as in Alzheimer’s disease, the consequences can be devastating. Understanding the neurobiology of memory will help develop treatments for patients with memory loss. Here we describe the myriad processes involved in memory consolidation, including cholinergic and dopaminergic neurotransmission predominantly in hippocampal networks. We discuss established therapies as well as potential novel strategies for boosting cognition. Future approaches to enhancement of memory consolidation include not only pharmacological and neurosurgical treatments, but also lifestyle interventions — for example, modifications to sleep, exercise and diet.</jats:p

Motor neglect associated with loss of action inhibition

Motor neglect, underuse of one side of the body not explained by weakness or sensory impairment, is a common consequence of stroke that is surprisingly little understood. Behavioural and neuroanatomical hallmarks of the disorder are investigated. Using a masked prime task, it was shown that when patients with left motor neglect plan to move their left hand, irrelevant right limb motor programmes intrude, causing delay. Lesion analysis reveals that such asymmetry of motor programming occurs after infarcts of the right putamen and motor association areas. This demonstration of failure to inhibit ipsilesional limb motor plans suggests potential benefit from interventions that might act to restore balance in action planning

In search of ‘lost’ knowledge and outsourced expertise in flood risk management

This paper examines the parallel discourses of ‘lost’ local flood expertise and the growing use of commercial consultancies to outsource aspects of flood risk work. We critically examine the various claims and counter-claims about lost, local and external expertise in flood management, focusing on the aftermath of the 2007 floods in East Yorkshire, England. Drawing on interviews with consultants, drainage engineers and others, we caution against claims that privilege ‘local’ floods knowledge as ‘good’ and expert knowledge as somehow suspect. This paper urges carefulness in interpreting claims about local knowledge, arguing that it is important always to think instead of hybrid knowledge formations. We conclude by arguing that experiments in the co-production of flood risk knowledge need to be seen as part of a spectrum of ways for producing shared knowledge

Visual neglect after right posterior cerebral artery infarction

This article has been made available through the Brunel Open Access Publishing Fund and is available from the specified link - Copyright © 2006 BMJ Publishing Group.Objectives: To investigate the characteristics and neuroanatomical correlates of visual neglect after right-sided posterior cerebral artery (PCA) infarction.Methods: 15 patients with acute PCA strokes were screened for the presence of neglect on a comprehensive battery of cognitive tests. Extra tests of visual perception were also carried out on six patients. To establish which areas were critically associated with neglect, the lesions of patients with and without neglect were compared.Results: Neglect of varying severity was documented in 8 patients. In addition, higher-order visual perception was impaired in 5 of the 6 patients. Neglect was critically associated with damage to an area of white matter in the occipital lobe corresponding to a white matter tract connecting the parahippocampal gyrus with the angular gyrus of the parietal lobe. Lesions of the thalamus or splenium of the corpus callosum did not appear necessary or sufficient to cause neglect, but may mediate its severity in these patients.Conclusions: PCA stroke can result in visual neglect. Interruption of the white matter fibres connecting the parahippocampal gyrus to the angular gyrus may be important in determining whether a patient will manifest neglect

APOE ε4, Alzheimer's disease neuropathology, and sleep disturbance, in individuals with and without dementia

BACKGROUND: Apolipoprotein E epsilon 4 (APOE-ε4) carrier status is an established risk factor for Alzheimer’s disease (AD) dementia. It has also been linked with sleep disturbance in healthy older adults and increased insomnia risk. This association may be driven by the effect of APOE-ε4 on AD pathological change, itself associated with sleep abnormalities. To assess this relationship, we have evaluated post-mortem neuropathological findings in patients with and without cognitive impairment and AD pathology, who had extensive clinical assessment within 12 months of death. METHODS: This retrospective cohort study used UK Brain Banks Network data. Eligible subjects were aged over 50, with pre-mortem neuropsychiatry inventory scores of sleep disturbance (NPI-K), neurocognitive testing and functional cognitive status assessment (Clinical Dementia Rating scale). Neuropathological data included Thal phase, Braak stage and CERAD scores (measures of Aβ plaque distribution, tangle distribution and neuritic plaque density, respectively) combined to form the National Institute on Aging Alzheimer’s Association (NIA-AA) ABC score reflecting AD neuropathology. Participants with other significant intracerebral pathology or pathological features of non-AD dementia were excluded. Multivariate linear regression was performed with NPIK Global Score (NPIK frequency score multiplied by severity score) as the dependent variable and APOE-ε4 heterozygosity or homozygosity as independent variables. Covariates included age, gender, APOE-ε2 status and ABC NPI measures reflecting depression and anxiety. Further models stratified by ABC score and functional cognitive status were also produced. RESULTS: Seven hundred twenty-eight records were identified. Two hundred two participants were included in the final analysis: mean (SD) age 84.0 (9.2) and MMSE 14.0 (11.8). Mean sleep disturbance scores were highest in ε4 homozygosity (n=11), 4.55 (5.4); intermediate in ε4 heterozygosity (n=95), 2.03 (4.0); and lowest in non-ε4 carriers (n=96), 1.36 (3.3). Within the full sample, controlling for pathological status, age, gender, depression, anxiety and CDR-SOB status, APOE-ε4 homozygosity was associated with sleep disturbance (β 2.53, p=0.034). APOE-ε4 heterozygosity was similarly associated in individuals without dementia (β 1.21, p=0.048). CONCLUSION: These findings lend weight to the hypothesis that APOE-ε4 affects sleep by mechanisms independent of AD pathological change. Evaluation of those mechanisms would enhance understanding of sleep disturbance pathways and potentially provide treatment targets. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13195-022-00992-y