The diagnostic value of tau protein, β-amyloid (1-42) and their ratio for the discrimination of alcohol-related cognitive disorders from Alzheimer's disease in the early stages

2005 ◽  
Vol 20 (8) ◽  
pp. 722-729 ◽  
Author(s):  
Elisabeth Kapaki ◽  
Ioannis Liappas ◽  
George P. Paraskevas ◽  
Ilia Theotoka ◽  
Andreas Rabavilas
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Cognitive Disorders ◽  
Diagnostic Value ◽  
Early Stages ◽  
Β Amyloid

scholarly journals Intracerebral Injection of Extracellular Vesicles from Mesenchymal Stem Cells Exerts Reduced Aβ Plaque Burden in Early Stages of a Preclinical Model of Alzheimer’s Disease

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1059 ◽  
Author(s):  
Chiara A. Elia ◽  
Matteo Tamborini ◽  
Marco Rasile ◽  
Genni Desiato ◽  
Sara Marchetti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Clinical Manifestations ◽  
Plaque Burden ◽  
Intracerebral Injection ◽  
Early Stages ◽  
Β Amyloid

Bone marrow Mesenchymal Stem Cells (BM-MSCs), due to their strong protective and anti-inflammatory abilities, have been widely investigated in the context of several diseases for their possible therapeutic role, based on the release of a highly proactive secretome composed of soluble factors and Extracellular Vesicles (EVs). BM-MSC-EVs, in particular, convey many of the beneficial features of parental cells, including direct and indirect β-amyloid degrading-activities, immunoregulatory and neurotrophic abilities. Therefore, EVs represent an extremely attractive tool for therapeutic purposes in neurodegenerative diseases, including Alzheimer’s disease (AD). We examined the therapeutic potential of BM-MSC-EVs injected intracerebrally into the neocortex of APPswe/PS1dE9 AD mice at 3 and 5 months of age, a time window in which the cognitive behavioral phenotype is not yet detectable or has just started to appear. We demonstrate that BM-MSC-EVs are effective at reducing the Aβ plaque burden and the amount of dystrophic neurites in both the cortex and hippocampus. The presence of Neprilysin on BM-MSC-EVs, opens the possibility of a direct β-amyloid degrading action. Our results indicate a potential role for BM-MSC-EVs already in the early stages of AD, suggesting the possibility of intervening before overt clinical manifestations.

The role of neurovascular unit damage in the occurrence and development of Alzheimer’s disease

2019 ◽  
Vol 30 (5) ◽  
pp. 477-484 ◽  
Author(s):  
Xin Liu ◽  
DeRen Hou ◽  
FangBo Lin ◽  
Jing Luo ◽  
JingWen Xie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Senile Dementia ◽  
Neurovascular Unit ◽  
Common Type ◽  
Pathological Changes ◽  
Β Amyloid ◽  
Progressive Cognitive Impairment

Abstract Alzheimer’s disease (AD) is a neurodegenerative disease with progressive cognitive impairment. It is the most common type of senile dementia, accounting for 65%–70% of senile dementia [Alzheimer’s Association (2016). 2016 Alzheimer’s disease facts and figures. Alzheimers Dement. 12, 459–509]. At present, the pathogenesis of AD is still unclear. It is considered that β-amyloid deposition, abnormal phosphorylation of tau protein, and neurofibrillary tangles are the basic pathological changes of AD. However, the role of neurovascular unit damage in the pathogenesis of AD has been attracting more and more attention in recent years. The composition of neurovascular unit and the role of neurovascular unit damage in the occurrence and development of AD were reviewed in this paper.

scholarly journals Modulation of glucose metabolism and metabolic connectivity by β-amyloid

2016 ◽  
Vol 36 (12) ◽  
pp. 2058-2071 ◽  
Author(s):  
Felix Carbonell ◽  
Alex P Zijdenbos ◽  
Donald G McLaren ◽  
Yasser Iturria-Medina ◽  
Barry J Bedell ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Metabolism ◽  
Disease Process ◽  
Continuous Variable ◽  
Amyloid Burden ◽  
Early Stages ◽  
Metabolic Connectivity ◽  
Β Amyloid ◽  
Glucose Hypometabolism

Glucose hypometabolism in the pre-clinical stage of Alzheimer’s disease (AD) has been primarily associated with the APOE ɛ4 genotype, rather than fibrillar β-amyloid. In contrast, aberrant patterns of metabolic connectivity are more strongly related to β-amyloid burden than APOE ɛ4 status. A major limitation of previous studies has been the dichotomous classification of subjects as amyloid-positive or amyloid-negative. Dichotomous treatment of a continuous variable, such as β-amyloid, potentially obscures the true relationship with metabolism and reduces the power to detect significant changes in connectivity. In the present work, we assessed alterations of glucose metabolism and metabolic connectivity as continuous function of β-amyloid burden using positron emission tomography scans from the Alzheimer’s Disease Neuroimaging Initiative study. Modeling β-amyloid as a continuous variable resulted in better model fits and improved power compared to the dichotomous model. Using this continuous model, we found that both APOE ɛ4 genotype and β-amyloid burden are strongly associated with glucose hypometabolism at early stages of Alzheimer’s disease. We also determined that the cumulative effects of β-amyloid deposition result in a particular pattern of altered metabolic connectivity, which is characterized by global, synchronized hypometabolism at early stages of the disease process, followed by regionally heterogeneous, progressive hypometabolism.

scholarly journals Elevating the Levels of Calcium Ions Exacerbate Alzheimer’s Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau

2021 ◽  
Vol 22 (11) ◽  
pp. 5900
Author(s):  
Pei-Pei Guan ◽  
Long-Long Cao ◽  
Pu Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Calcium Ions ◽  
Tau Protein ◽  
Learning Ability ◽  
Amyloid Protein ◽  
Aβ Peptides ◽  
High Incidence ◽  
High Incidence Rate ◽  
Β Amyloid

Alzheimer’s disease (AD) is a neurodegenerative disease with a high incidence rate. The main pathological features of AD are β-amyloid plaques (APs), which are formed by β-amyloid protein (Aβ) deposition, and neurofibrillary tangles (NFTs), which are formed by the excessive phosphorylation of the tau protein. Although a series of studies have shown that the accumulation of metal ions, including calcium ions (Ca2+), can promote the formation of APs and NFTs, there is no systematic review of the mechanisms by which Ca2+ affects the development and progression of AD. In view of this, the current review summarizes the mechanisms by which Ca2+ is transported into and out of cells and organelles, such as the cell, endoplasmic reticulum, mitochondrial and lysosomal membranes to affect the balance of intracellular Ca2+ levels. In addition, dyshomeostasis of Ca2+ plays an important role in modulating the pathogenesis of AD by influencing the production and aggregation of Aβ peptides and tau protein phosphorylation and the ways that disrupting the metabolic balance of Ca2+ can affect the learning ability and memory of people with AD. In addition, the effects of these mechanisms on the synaptic plasticity are also discussed. Finally, the molecular network through which Ca2+ regulates the pathogenesis of AD is introduced, providing a theoretical basis for improving the clinical treatment of AD.

Mechanisms of Melatonin Binding and Destabilizing Protofilament and Filament of Tau R3-R4 Domains Revealed by Molecular Dynamics Simulation

2021 ◽  
Author(s):  
Lili Zhu ◽  
Yehong Gong ◽  
Hao Lju ◽  
Gongwu Sun ◽  
Qingwen Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Dynamics ◽  
Molecular Dynamics Simulation ◽  
Tau Protein ◽  
Dynamics Simulation ◽  
Pathological Characteristics ◽  
Amyloid Aβ ◽  
Β Amyloid

The accumulations of β-amyloid (Aβ) and tau protein are considered as two important pathological characteristics of Alzheimer's disease (AD). Failures of medicine targeting Aβ have drawn more attention to tau...

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