Current Alzheimer research
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The analysis of the facial expression of pain promises to be one of the most sensitive tools for the detection of pain in patients with moderate to severe forms of dementia, who can no longer self-report pain. Fine-grain analysis using the Facial Action Coding System (FACS) is possible in research but not feasible for clinical use at the moment because it is too time and effort consuming. Studies using the FACS showed either enhanced facial responses or no alterations of facial activity during pain in patients with cognitive impairment. ⋯ Despite this agreement, the content of these face items is very different, ranging from anatomically-based descriptions to inference of internal states. Recent studies let the anatomical orientation appear more promising. Automated video systems for the detection of pain in patients with dementia may lead to ground-breaking improvements of pain care in the future.
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Review Meta Analysis
Cerebral Microinfarcts and Dementia: A Systematic Review and Metaanalysis.
To systematically review the relationship between the cerebral microinfarcts and dementia. ⋯ These results suggest that cerebral microinfarcts are significantly associated with dementia. Whether cerebral microinfarcts are associated with AD needs to be further investigated.
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Under-assessment and inadequate treatment of pain is a common problem for older adults, particularly those with dementia. This may be in part attributed to knowledge deficits and negative attitudes among healthcare staff and informal caregivers towards pain, its assessment and its management in dementia. Knowledge and attitudes have a significant predictive relationship with behavior, potentially impacting pain assessment and management practices. ⋯ Understanding and positive attitudes were demonstrated in some areas, such as non-narcotic pain medications and identifying behavioral pain indicators. Of the 4 scales identified, positive results were found for internal consistency and content validity, however further refinement and testing is necessary. It was concluded attitudinal and knowledge barriers exist which should be addressed given their influence over practice behavior, however, there is a willingness and knowledge base from which progress can build.
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The early phase of Alzheimer`s disease (AD) involves the disruption of finely tuned neuronal circuitry in brain regions associated with learning and memory. This tuning is obtained from the delicate balance of excitatory and inhibitory inputs which regulate cortical network function. This homeostatic plasticity provides a dynamic basis for appropriate information transfer in the brain. Excitatory synaptic transmission is driven mainly by glutamatergic synapses whereas inhibitory synaptic transmission involves GABAergic and glycinergic signaling. GABAergic cells, responsible for inhibitory transmission in adult brain, have recently become the subject of study in AD research. The discovery that GABAergic interneurons are targets of the amyloid-beta (Aβ) peptide suggest that deregulation of the excitatory/inhibitory balance contributes to changes in cortical regulation, possibly with consequences for the development of the pathology. Thus, understanding the molecular details involved in GABAergic alterations may provide insight into the pathogenesis of AD. ⋯ We look at approaches that may lead to new hypotheses, animal models and therapeutic strategies based on GABAergic cells in AD with particular interest in microcircuits.
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Review
Calcium signalling toolkits in astrocytes and spatio-temporal progression of Alzheimer's disease.
Pathological remodelling of astroglia represents an important component of the pathogenesis of Alzheimer's disease (AD). In AD astrocytes undergo both atrophy and reactivity; which may be specific for different stages of the disease evolution. Astroglial reactivity represents the generic defensive mechanism, and inhibition of astrogliotic response exacerbates b-amyloid pathology associated with AD. ⋯ Reactive astrogliosis is linked to astroglial Ca(2+) signalling, this latter being widely regarded as a mechanism of astroglial excitability. The AD pathology evolving in animal models as well as acute or chronic exposure to β-amyloid induce pathological remodelling of Ca(2+) signalling toolkit in astrocytes. This remodelling modifies astroglial Ca(2+) signalling and may be linked to cellular mechanisms of AD pathogenesis.