|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Most of the research on Alzheimer's disease focuses on the correlation of its neuropathological changes in the neurofibrillary tangles caused by hyper-phosphorylated tau protein and β-amyloid plaques with respect to cognitive impairment.
|
31695992 |
2019 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
These findings suggest that (1) LB pathology can influence the clinical features of familial AD, (2) the E184D mutation of presenilin-1 may be associated with the LB formation through Abeta overproduction, although the process of LB formation is strongly affected by other unknown mechanisms, (3) in neurodegenerative disorders with LBs, there is a common pathophysiological background inducing NAC accumulation in neuritic plaques and astrocytes, and (4) the NAC accumulation in neuritic plaques is modulated by the abnormally aggregated tau protein.
|
12410385 |
2002 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
An excess of senile plaques (beta-amyloid protein) and neurofibrillary tangles (tau protein), ventricular enlargement, and cortical atrophy characterizes it.
|
16246446 |
2005 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Thus, tau mutations cause FTDP-17 by multiple pathological mechanisms, which may explain the phenotypic heterogeneity observed in FTDP-17, as exemplified by an unusual family described here with tau pathology as well as amyloid and neuritic plaques.
|
10318930 |
1999 |
|
Senile Plaques
|
0.200 |
PosttranslationalModification
|
disease |
BEFREE |
The major changes include the formation of senile plaques and neurofibrillary tangles primarily owing to the deposition of amyloid β plaques (Aβ) and hyper-phosphorylation of tau protein.
|
29183770 |
2018 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
The pathological hallmarks are extracellular deposits of amyloid plaques and intracellular neurofibrillary tangles of tau protein.
|
29274586 |
2018 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
It has now been ~ 30 years since the Alzheimer's disease (AD) research entered what may be termed the 'molecular era' that began with the identification of the amyloid β protein (Aβ) as the primary component of amyloid within senile plaques and cerebrovascular amyloid and the microtubule-associated protein tau as the primary component of neurofibrillary tangles in the AD brain.
|
27145445 |
2016 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD), the most common chronic neurodegenerative disease, is pathologically characterized by the formation of neurofibrillary tangles because of hyperphosphorylation of tau protein and extracellular deposits of amyloid-β (Aβ) protein termed senile plaques.
|
29200096 |
2018 |
|
Senile Plaques
|
0.200 |
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 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD) is known to be caused by the accumulation of deformed beta amyloid and hyperphosphorylated tau proteins resulting into formation and aggregation of senile plaques and neurofibrillary tangles in the brain.
|
29377514 |
2018 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
The formation of senile plaques and neurofibrillary tangles of the tau protein are the main pathological mechanism of Alzheimer's disease (AD).
|
29338678 |
2019 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
The accumulation of β-amyloid plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein are two hallmarks of AD.
|
30964647 |
2019 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Further, since intracerebral injections of PHF tau with and without AlCl3 in rats appear uniquely capable of inducing co-deposits of a number of proteins found in authentic AD SPs and NFTs (including A beta, ubiquitin, ACT, and ApoE), we speculate that the contributions of PHF tau to plaque and tangle formation in AD may be modulated by aluminum.
|
7525898 |
1994 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
A central event in Alzheimer's disease is the conformational change from normally circulating soluble amyloid beta peptides (A beta) and tau proteins into amyloid fibrils, in the form of senile plaques and neurofibrillary tangles respectively.
|
7534068 |
1995 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Biochemical modifications of tau proteins have been proposed to be among the earliest neurobiological changes in Alzheimer's disease (AD) and correlate better with cognitive symptoms than do beta-amyloid plaques.
|
18511295 |
2008 |
|
Senile Plaques
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The senile plaques (SPs) and neurofibrillary tangles (NFTs) are the two major pathological hallmarks of AD, which are composed of β-amyloid protein and Tau protein.
|
28623460 |
2017 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by neuritic plaques (main constituent: β-amyloid [Aβ]) and neurofibrillary tangles (hyperphosphorylated tau protein) in the brain.
|
22917148 |
2012 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
In some places plaques bore a resemblance to senile neuritic plaques and in the hippocampus there were abundant typical neuritic plaques giving positive staining reactions for beta-amyloid protein and tau protein, but not PrP.
|
8513392 |
1993 |
|
Senile Plaques
|
0.200 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD) is a complex neurodegenerative disorder pathologically identified by the presence of extracellular senile plaques (SP) with a proteinaceous core composed of aggregates of the amyloid peptide (Abeta) and intracellular aggregates of the microtubule-associated protein tau (tau) as neurofibrillary tangles (NFTs).
|
17017867 |
2006 |