The worldwide economic impact of dementia 2010

Wimo, Anders; Jönsson, Linus; Bond, John; Prince, Martin; Winblad, Bengt

doi:10.1016/j.jalz.2012.11.006

Cited by 1,001 publications

(921 citation statements)

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“…3,4,[11][12][13][14][15][16] Moreover, the incident of dementia after recurrent stroke was 33.33 %. 11 Factors independently associated with dementia in stroke patients were as follows: atrial fibrillation, the previous stroke, myocardial infarction, hypertension, diabetes mellitus, and the previous transient ischemic attack.…”

Section: Discussionmentioning

confidence: 99%

“…3,4 Moreover, probability of recurrent stroke increased, 9,10 recurrent stroke was 33.3 percentage, 11 the mortality rate of dementia after stroking was three times compared with and without, 7 and the estimated cost of caring the dementia patients around the world is approximately 604,000 million US dollar. 12 Mechanism of disease, symptoms and risk factors, and mechanisms of post-stroke dementia may be the direct consequence of the vascular lesions of the brain. Second, post-stroke dementia may be caused by an associated asymptomatic Alzheimer pathology.…”

Section: Introductionmentioning

confidence: 99%

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Risk factors associated with post-stroke dementia: a systematic review and meta-analysis

et al. 2017

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This study aimed to evaluate the risk factors for prognostic of post-stroke dementia (PSD). A systematic review included case-control and/or cohort studies, we searched both published and unpublished literatures between 2000 to July 31, 2016. Two authors independently screened and selected research articles. If another one disagreed, the third author would be just along with his/her professionally. Moreover, Critical appraisal was measured by the quality (GRADE). Data collection was in the data extraction form. The Rev-Man 5.3 was used to estimate pooled data. The fixed-effect model will be used when the heterogeneity I² <50%, whereas the random-effects model will be used when the heterogeneity I²>50%. Result eight publications were pooled for measuring an association between risk factors and PSD by meta-analysis. There were 6 strongly PSD risk factors. The pooled relative ratio (RR) of atrial fibrillation was 1.68, previous stroke 1.59, myocardial infarction 1.40, hypertension 1.36, diabetes mellitus 1.25 and previous transient ischemic attack 1.25 respectively. Un-pooled data from 13 publications reported that the risk factors for dementia in stroke patients were i) demographic factors, ii) vascular risk factors, iii) stroke factors, iv) stroke complications, and v) abnormalities on brain imaging. Strongly risk factors associated with increasing PSD risk were atrial fibrillation, previous stroke, myocardial infarction, hypertension, diabetes mellitus, and previous transient ischemic attack. Further studies, strongly risk factors need to investigate and develop the risk score for the prediction of dementia in stroke patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Risk factors associated with post-stroke dementia: a systematic review and meta-analysis

et al. 2017

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“…Alzheimer's disease (AD) is the most common form of dementia, with an estimated 37 million sufferers worldwide and is expected to affect 115 million by 2050 if no effective therapeutic strategies are developed (Wimo et al, 2013). The enormous worldwide costs of dementia are expected to rise in the next few years.…”

Section: Introductionmentioning

confidence: 99%

Detection of the tau protein in human serum by a sensitive four-electrode electrochemical biosensor

Wang

Acha

Shah

et al. 2017

Biosensors and Bioelectronics

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This study presents a novel approach based on a four-electrode electrochemical biosensor for the detection of tau protein -one of the possible markers for the prediction of Alzheimer's disease (AD). The biosensor is based on the formation of stable antibody-antigen complexes on gold microband electrodes covered with a layer of a self-assembled monolayer and protein G. Antibodies were immobilized on the gold electrode surface in an optimal orientation by protein G interaction. Electrochemical impedance spectroscopy was used to analyze impedance change, which revealed a linear response with increasing tau concentrations. The assay is fast (<1 h for incubation and measurement) and very sensitive. The limit of quantification for the full-length 2N4R tau protein is 0.03 pM, a value unaltered when the assay was processed in bovine serum albumin or human serum. This technology could be adapted for the detection of other biomarkers to provide a multiple assay to identify AD progression in a point of care setting.

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“…Currently four million individuals in the United States Cindy Beharry, et al Tau-induced neurodegeneration: mechanisms and targets 347 alone are affected and it has been estimated to cost the world $604 billion in 2010 [2,19] . Currently, there is no cure for AD and available drugs have been unable to intervene in the disease process enough to prevent or cure it [2] .…”

Section: Introductionmentioning

confidence: 99%

“…Tau is a phosphoprotein that is encoded by a single gene, MAPT, located on chromosome 17q21 [16] ; alternative splicing of the gene produces six major isoforms expressed in the adult human brain [17] . Isoforms derive their names from the number of microtubule-binding repeat sequences and which N-terminal exons are included [18] .Currently four million individuals in the United States Cindy Beharry, et al Tau-induced neurodegeneration: mechanisms and targets 347 alone are affected and it has been estimated to cost the world $604 billion in 2010 [2,19] . Currently, there is no cure for AD and available drugs have been unable to intervene in the disease process enough to prevent or cure it [2] .…”

mentioning

confidence: 99%

Tau-induced neurodegeneration: mechanisms and targets

Beharry

Cohen

et al. 2014

Neurosci. Bull.

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The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau's functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifi cations can alter tau's biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.Keywords: tau; phosphorylation; neurodegeneration; tauopathies; mitochondria; microtubules; tubulin; kinases; phosphatases; Alzheimer's disease ·Review· IntroductionAlzheimer 's disease (AD), first described by Alois Alzheimer more than 100 years ago [1] , is a progressive neurodegenerative disorder, characterized by an insidious onset with irreversible cognitive declines that lead to profound mental deterioration causing dementia [2] . Two major forms of lesion characterize AD: amyloid as diffuse neurotic plaques primarily composed of the Aβ peptide [3] , which are mainly insoluble deposits of protein and cellular material, and neurofibrillary tangles composed of fi lamentous hyperphosphorylated tau protein that builds up inside the neuron [4,5] .Amyloid precursor protein (APP) is a highly conserved transmembrane protein [6] believed to play a role in synapse formation, synaptic plasticity, and neuronal survival [7][8][9] .In AD, APP is cleaved by β-and γ-secretases leading to the overproduction of an abnormal proteolytic byproduct called amyloid beta (Aβ) [10] . Upon cleavage fragments of Aβ of various sizes are released from the membrane and aggregate in the brain to form the characteristic plaques seen in AD. Plaques are composed primarily of the 40 and 42 amino-acid peptide fragments Aβ40 and Aβ42, the latter being the predominant species. In addition, Aβ42 is more prone to aggregation and deposition and therefore the cause of neurotoxicity, as well as synaptic loss [11] .The second lesion in AD is formed by aggregates of the microtubule-associated protein tau, which forms intracytoplasmic neuronal inclusions or neurofibrillary tangles when hyperphosphorylated [12] . Tau is associated with neurons of the central nervous system [13] and its main biological function is promoting the in vitro assembly and stabilization of microtubules in the cytoskeleton [14,15] . Tau is a phosphoprotein that is encoded by a single gene, MAPT, located on chromosome 17q21 [16] ; alternative splicing of the gene produces six major isoforms expressed in the adult human brain [17] . Isoforms derive their names from the number of microtubule-binding repeat s...

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The worldwide economic impact of dementia 2010

Cited by 1,001 publications

References 73 publications

Risk factors associated with post-stroke dementia: a systematic review and meta-analysis

Risk factors associated with post-stroke dementia: a systematic review and meta-analysis

Detection of the tau protein in human serum by a sensitive four-electrode electrochemical biosensor

Tau-induced neurodegeneration: mechanisms and targets

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