An exploration of the representational culture of
Alzheimer's disease and how media technologies shape our ideas of
cognition and aging
With no known cause or cure despite a century of research,
...Alzheimer's disease is a true medical mystery. In Mediating
Alzheimer's , Scott Selberg examines the nature of this
enduring national health crisis by looking at the disease's
relationship to media and representation. He shows how collective
investments in different kinds of media have historically shaped
how we understand, treat, and live with this disease.
Selberg demonstrates how the cognitive abilities that
Alzheimer's threatens-memory, for example-are integrated into the
operations of representational technologies, from Polaroid
photographs to Post-its to digital artificial intelligence.
Focusing on a wide variety of media technologies, such as
neuroimaging, art therapy, virtual reality, and social media, he
shows how these cognitively oriented media ultimately help define
personhood for people with Alzheimer's. Media have changed the
practices of successful aging in the United States, and Selberg
takes us deep into how technologies like digital brain-training and
online care networks shape ideas of cognition and healthy
aging.
Packed with startlingly fresh insights, Mediating
Alzheimer's contributes to debates around bioethics, the labor
of caregiving, and a national economy increasingly invested in
communication and digital media. Probing the very technologies that
promise to save and understand our brains, it gives us new ways of
understanding Alzheimer's disease and aging in America.
Low and high concentrations of plasma magnesium are associated with increased risk of future all-cause dementia; however, the underlying reasons remain elusive. The magnesium ion is an important ...electrolyte serving as a cofactor in many enzymatic processes in the human organism. Magnesium affects both neuronal and vascular functions. We investigated the associations of plasma concentrations of magnesium associate with common subtypes of dementia as Alzheimer dementia and non-Alzheimer dementia, and potential pathways by which magnesium may affect risk of dementia.
Plasma concentrations of magnesium were measured in 102 648 individuals from the Copenhagen General Population Study. Cox regression and natural effects mediation analyses evaluated associations with either Alzheimer dementia or non-Alzheimer dementia.
Multifactorially adjusted hazard ratios for non-Alzheimer dementia were 1.50(95% confidence interval (CI):1.21-1.87) for the lowest and 1.34(1.07-1.69) for the highest vs the fourth quintile (reference) of plasma magnesium concentrations. Diabetes, cumulated smoking, stroke, and systolic blood pressure mediated 10.4%(3.1-22.8%), 6.8%(1.2-14.0%), 1.3%(0.1-3.6%), and 1.0%(0.2-2.6%), respectively, in the lowest quintile, whereas stroke mediated 3.2%(0.4-11.9%) in the highest quintile. No associations were observed for Alzheimer dementia.
Low and high plasma magnesium concentrations were associated with high risk of vascular-related non-Alzheimer dementia, with the lowest risk observed at a concentration of 2.07 mg/dL (0.85 mmol/L). No association was observed for Alzheimer dementia. Mediation analysis suggested that diabetes may be in the causal pathway between low plasma magnesium concentrations and high risk of non-Alzheimer dementia, while cumulated smoking, stroke, and systolic blood pressure played minor mediating roles.
ALZHEIMER’S DEMENTIA AND ORAL HEALTH OF ELDERLY Dana-Gabriela Budală; Zinovia Surlari; Dragoș Ioan Virvescu ...
Romanian Journal of Medical and Dental Education (Online),
08/2021, Volume:
10, Issue:
4
Journal Article
Peer reviewed
Open access
The improvement of the basic properties of dental restorative materials, such as their mechanical, physical, aesthetic, and bonding properties, has been dramatic and the current materials on the ...market show excellent clinical performance. This review article compiles the characteristics of ceramic dentures materials and the efforts made in order to improve the main features and to point out future perspectives.
Studies have reported a protective relation to cognitive decline with long-term intake of total and individual dietary carotenoids. However, the underlying mechanisms have not yet been clearly ...established in humans.
To evaluate the prospective association between intakes of total and individual carotenoids and risk of incident Alzheimer dementia (AD) and explore the underlying neuropathological basis.
Among 927 participants from the Rush Memory and Aging Project who were free from AD at baseline and were followed up for a mean of 7 y, we estimated HRs for AD using Cox proportional hazards models by intakes of energy-adjusted carotenoids. Brain AD neuropathology was assessed in postmortem brain autopsies among 508 deceased participants. We used linear regression to assess the association of carotenoid intake with AD-related neuropathology.
Higher intake of total carotenoids was associated with substantially lower hazard of AD after controlling for age, sex, education, ApoE-ε4, participation in cognitively stimulating activities, and physical activity level. Comparing the top and bottom quintiles (median intake: 24.8 compared with 6.7 mg/d) of total carotenoids, the multivariate HR (95% CI) was 0.52 (0.33, 0.81), P-trend < 0.01. A similar association was observed for lutein-zeaxanthin, a weaker linear inverse association was observed for β-carotene, and a marginally significant linear inverse association was found for β-cryptoxanthin. Among the deceased participants, consumers of higher total carotenoids (top compared with bottom tertile, 18.2 compared with 8.2 mg/d) had less global AD pathology (b: −0.10; SE = 0.04; P-trend = 0.01). For individual carotenoids, lutein-zeaxanthin and lycopene were inversely associated with brain global pathology, whereas lutein-zeaxanthin showed additional inverse associations with AD diagnostic score, neuritic plaque severity, and neurofibrillary tangle density and severity.
Our findings support a beneficial role of total carotenoid consumption, in particular lutein/zeaxanthin, on AD incidence that may be related to the inhibition of brain β-amyloid deposition and fibril formation.
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CMK, GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Alterations in the concentrations of trace elements may play a vital role in Alzheimer dementia progression. However, previous research results are inconsistent, and there is still a lack of review ...on the relationship between all the studied-trace elements and AD from various perspectives of population-based studies. In this study, we systematically reviewed previous population-based studies and identified the altered trace elements in AD patients. We searched the Web of Science Core Collection, PubMed, and Scopus database, and ultimately included 73 articles. A bibliometric analysis was conducted to explore the evolution of the field from an epidemiological perspective. Bibliometric data such as trace elements, biological materials, detection methods, cognitive tests, co-occurrence and co-citation statistics are all analyzed and presented in a quantitative manner. The 73 included studies analyzed 39 trace elements in total. In a further meta-analysis, standardized mean differences (SMDs) of 13 elements were calculated to evaluate their altered in AD patients, including copper, iron, zinc, selenium, manganese, lead, aluminum, cadmium, chromium, arsenic, mercury, cobalt, and manganese. We identified four trace elements—copper (serum), iron (plasma), zinc (hair), and selenium (plasma)—altered in AD patients, with SMDs of 0.37 (95% confidence interval CI: 0.10, 0.65), −0.68 (95% CI: −1.34, −0.02), −0.35 (95% CI: −0.62, −0.08), and −0.61 (95% CI: −0.97, −0.25), respectively. Finally, we formed a database of various trace element levels in AD patients and healthy controls. Our study can help future researchers gain a comprehensive understanding of the advancements in the field, and our results provide comprehensive population-based data for future research.
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•Innovatively combines bibliometric and meta-analysis methods.•Quantifying the evolution of population studies from epidemiological perspective.•Cu, Fe, Zn, and Se were identified as significantly altered in AD patients.•Trace element database for various tissues of AD patients was established.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
ABSTRACTThe neuropathologic examination is considered to provide the gold standard for Alzheimer disease (AD). To determine the accuracy of currently used clinical diagnostic methods, clinical and ...neuropathologic data from the National Alzheimer’s Coordinating Center, which gathers information from the network of National Institute on Aging (NIA)-sponsored Alzheimer Disease Centers (ADCs), were collected as part of the National Alzheimer’s Coordinating Center Uniform Data Set (UDS) between 2005 and 2010. A database search initially included all 1198 subjects with at least one UDS clinical assessment and who had died and been autopsied; 279 were excluded as being not demented or because critical data fields were missing. The final subject number was 919. Sensitivity and specificity were determined based on “probable” and “possible” AD levels of clinical confidence and 4 levels of neuropathologic confidence based on varying neuritic plaque densities and Braak neurofibrillary stages. Sensitivity ranged from 70.9% to 87.3%; specificity ranged from 44.3% to 70.8%. Sensitivity was generally increased with more permissive clinical criteria and specificity was increased with more restrictive criteria, whereas the opposite was true for neuropathologic criteria. When a clinical diagnosis was not confirmed by minimum levels of AD histopathology, the most frequent primary neuropathologic diagnoses were tangle-only dementia or argyrophilic grain disease, frontotemporal lobar degeneration, cerebrovascular disease, Lewy body disease and hippocampal sclerosis. When dementia was not clinically diagnosed as AD, 39% of these cases met or exceeded minimum threshold levels of AD histopathology. Neurologists of the NIA-ADCs had higher predictive accuracy when they diagnosed AD in subjects with dementia than when they diagnosed dementing diseases other than AD. The misdiagnosis rate should be considered when estimating subject numbers for AD studies, including clinical trials and epidemiologic studies.
The pathological processes leading to synapse loss, neuronal loss, brain atrophy and gliosis in Alzheimer's disease (AD) and their relation to vascular disease and immunological changes are yet to be ...fully explored. Amyloid‐β (Aβ) aggregation, vascular damage and altered immune response interact at the blood–brain barrier (BBB), affecting the brain endothelium and fuelling neurodegeneration. The aim of the present systematic literature review was to critically appraise and to summarise the published evidence on the clinical correlations and pathophysiological concepts of BBB damage in AD, focusing on human data. The PubMed, Cochrane, Medline and Embase databases were searched for original research articles, systematic reviews and meta‐analyses, published in English language from 01/2000 to 07/2021, using the keywords Alzheimer*, amyloid‐β or β‐amyloid or abeta and BBB. This review shows that specific changes of intercellular structures, reduced expression of transendothelial carriers, induction of vasoactive mediators and activation of both astroglia and monocytes/macrophages characterise BBB damage in human AD and AD models. BBB dysfunction on magnetic resonance imaging takes place early in the disease course in AD‐specific brain regions. The toxic effects of Aβ and apolipoprotein E (ApoE) are likely to induce a non‐cerebral‐amyloid‐angiopathy‐related degeneration of endothelial cells, independently of cerebrovascular disease; however, some of the observed structural changes may just arise with age. Small vessel disease, ApoE, loss of pericytes, proinflammatory signalling and cerebral amyloid angiopathy enhance BBB damage. Novel therapeutic approaches for AD, including magnetic resonance‐guided focused ultrasound, aim to open the BBB, potentially leading to an improved drainage of Aβ along perivascular channels and increased elimination from the brain. In vitro treatments with ApoE‐modifying agents yielded promising effects on modulating BBB function. Reducing cardiovascular risk factors represents one of the most promising interventions for dementia prevention at present. However, further research is needed to elucidate the connection of BBB damage and tau pathology, the role of proinflammatory mediators in draining macromolecules and cells from the cerebral parenchyma, including their contribution to cerebral amyloid angiopathy. Improved insight into these pathomechanisms may allow to shed light on the role of Aβ deposition as a primary versus a secondary event in the complex pathogenesis of AD.
The available evidence on BBB dysfunction in AD strongly suggests an interaction between Aβ deposition, clearance, vascular changes and dysregulation of the immune system. Non‐CAA‐ and non‐SVD‐related vasculopathic and proinflammatory effects of Aβ are likely to enhance disease progression. Further research is required to elucidate the interaction of cells at the neurovascular unit, downstream effects of the Aβ peptide and the role of co‐factors such as proinflammatory mediators in draining macromolecules from the cerebral parenchyma.
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DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK
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