|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We assessed whether these polymorphisms are associated with cerebrospinal fluid AD biomarkers including total tau (t-tau), phosphorylated tau proteins (p-tau181, p-tau199, and p-tau231), amyloid-β42 (Aβ42), and visinin-like protein 1 (VILIP-1) to test possible relationships of specific genotypes and pathological levels of CSF AD biomarkers.
|
31771069 |
2020 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
As a result, Aβ and Tau generate continually, which aggravates both autophagy dysfunction and AD.
|
31503421 |
2020 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The microtubule-associated protein tau regulates axonal transport of proteins, and tau deletion rescues Aβ-induced transport deficits in vitro.
|
31701556 |
2019 |
|
Amyloidosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In cortical regions of brains from individuals with preclinical or clinical Alzheimer's disease (AD), extracellular β-amyloid (Aβ) deposition precedes the aggregation of pathological intracellular tau (the product of the gene microtubule-associated protein tau (<i>MAPT</i>)).
|
31273083 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
One hundred fifty-three patients were recruited and tested for classical AD CSF biomarkers- Amyloid-ß42 and tau proteins - and novel candidate biomarkers - neurofilament (NF-) light and microRNA (miR) -21, -125b, -146a, and -222.All dementia patients had significantly higher concentrations of NF-light compared to CNS, with the TP group displaying the highest NF-light values.
|
31029057 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Changes in amyloid precursor protein (APP) cleavage and production of the APP fragment beta-amyloid (Aβ) along with hyperphosphorylated tau protein aggregation coalesce to cause reduction in synaptic strength, synaptic loss, and neurodegeneration.
|
31753135 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Based on the AT(N) (i.e., Amyloid/Tau/Neurodegeneration) pathological classification system, we classified subjects into four groups using cerebrospinal fluid amyloid-beta<sub>1-42</sub> (A) and phosphorylated tau protein<sub>181</sub> (T).
|
31029051 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The abnormal accumulation of amyloid-β and tau targets specific spatial networks in Alzheimer's disease.
|
31815669 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The AD-iN cultures that result have mature phenotypic and physiological properties, together with AD-like biochemical features that include extracellular β-amyloid (Aβ) accumulation and Tau protein phosphorylation.
|
31848379 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Different proteins (such as amyloid precursor protein (APP), β- amyloid (Aβ) and tau protein) play a key role in the initiation and progression of AD.
|
30605056 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alzheimer's Disease (AD) is an age-dependent neurodegenerative disorder, the most common type of dementia that is clinically characterized by the presence of beta-amyloid (Aβ) extracellularly and intraneuronal tau protein tangles that eventually leads to the onset of memory and cognition impairment, development of psychiatric symptoms and behavioral disorders that affect basic daily activities.
|
31642777 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The cognitive impairment caused by Alzheimer's disease (AD) is associated with beta-amyloid (Aβ) and tau proteins, and is accompanied by inflammation.
|
30408495 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD) comprises two major pathological hallmarks: extraneuronal deposition of β-amyloid (Aβ) peptides ("senile plaques") and intraneuronal aggregation of the microtubule-associated protein tau ("neurofibrillary tangles").
|
30261139 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Despite compelling evidence that the accumulation of amyloid-beta (Aβ) promotes neocortical MAPT (tau) aggregation in familial and idiopathic Alzheimer's disease (AD), murine models of cerebral amyloidosis are not considered to develop tau-associated pathology.
|
31673052 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Beta amyloid (Aβ) peptide aggregation and phosphorylated tau protein accumulation are considered as one of the causes for AD.
|
31482248 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
A threshold analysis was performed in 120 cognitively normal elderly individuals by modelling 2-year declines in brain glucose metabolism measured with [<sup>18</sup>F]fluorodeoxyglucose ([<sup>18</sup>F]FDG) as a function of [<sup>18</sup>F]florbetapir Aβ positron emission tomography (PET) and cerebrospinal fluid phosphorylated tau biomarker thresholds.
|
29396637 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The levels of phosphorylated p38 and phosphorylated tau protein at serine 202 in degenerated SK-N-MC cells were in the order: Aβ > (Aβ + RA-CUR) > (Aβ + 83-14 MAb-RA-CUR-PAAM-PLGA NPs) > (Aβ + 83-14 MAb-RA-CUR-PAAM-CL-PLGA NPs) ≈ control.
|
30033276 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Clinical value of CSF amyloid-beta-42 and tau proteins in Progressive Supranuclear Palsy.
|
29948175 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Beta-amyloid (Aβ) deposition and neurofibrillary tangles (NFTs) of abnormal hyperphosphorylated tau protein are the pathological hallmarks of the disease, accompanied by other pathological processes such as microglia activation.
|
30128693 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pathologically, patients with AD are characterized by deposition of senile plaques (SPs), formed by β-amyloid (Aβ), and neurofibrillary tangles (NTFs) that consist of aggregated hyperphosphorylated tau protein.
|
30003951 |
2018 |
|
Amyloidosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
There are many amounts of data supporting the view that AD pathogenesis so far there mainly are Aβ toxicity, tau protein, gene mutation, synaptic damages, intermediate neurons and network abnormalities, changes in mitochondrial function, chemokines, etc., Its nosogenesis may be involved in multiple theories and involved in multiple molecular signaling pathways, including Aβ, tau protein, and synaptic anomaly; mutual relationship between the mechanisms urge jointly neuronal degeneration.
|
29941717 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Also, recent studies demonstrate that alteration in endocytosis induces not only Aβ pathology but also the propagation of tau protein pathology, another key pathological feature of AD.
|
28697973 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
By affirming markers of abnormal Aβ and tau proteins as the essential pathobiological signature of Alzheimer's disease, the Framework tacitly reinforces the amyloid (Aβ) cascade as the leading theory of Alzheimer pathogenesis.
|
30220236 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
To define whether amyloid β protein deposits or tau protein lesions appear first during normal brain aging, we performed an immunohistological study on serial sections from 105 autopsy brains (age range: 40-104 years) from patients free of clinical signs of cognitive decline, using anti-tau (AT8) and anti-amyloid (4G8) antibodies in the hippocampus, entorhinal cortex, inferior temporal cortex (Brodmann area 20), prefrontal cortex (Brodmann area 9), occipital cortex (Brodmann areas 17 and 18), and in the brainstem.
|
29107845 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
CN, AVLT+, and AVLT- groups differed significantly on baseline brain (hippocampus, entorhinal cortex) and cerebrospinal fluid (amyloid, tau, p-tau) biomarkers, with the AVLT- group being most abnormal.
|
30511118 |
2018 |