PubMed 30046111

Staining for amyloid-β in the brains of nine patients with Alzheimer’s disease and eight controls without Alzheimer’s disease (Extended Data Table 1) revealed, as expected, marked parenchymal deposition of amyloid-β in the brains of patients with Alzheimer’s disease, but not in the brains of the controls without Alzheimer’s disease (Extended Data Fig. 9l, m)

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
8fdf6345d2
Confidence
Medium
MeSHAnatomy
Brain, Parenchymal Tissue
Networks

PubMed 30046111

Notably, when compared to tissue from controls, all samples from patients with Alzheimer’s disease demonstrated striking vascular amyloid-β pathology in the cortical leptomeninges (Extended Data Fig. 9l, m) and amyloid-β deposition in the dura mater adjacent to the superior sagittal sinus (Fig. 3i, j) or further away from the sinus (Fig. 3k, l)

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
aa1f1d007d
Confidence
Medium
MeSHAnatomy
Dura Mater, Superior Sagittal Sinus
Networks

PubMed 30046111

These findings showed that prominent meningeal amyloid-β deposition observed in patients with Alzheimer’s disease is also observed in mouse models of Alzheimer’s disease after meningeal lymphatic vessel ablation

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
879993d20e
Confidence
Medium
MeSHAnatomy
Meninges
MeSHDisease
Alzheimer Disease
Networks

PubMed 29196815

The histopathological changes in the brain include the presence of extracellular amyloid plaques consisted of various peptide variants of amyloid β (Aβ) and accumulation of intracellular neurofibrillary tangles (NFTs) composed mainly of phosphorylated Tau proteins (pTau), localized predominantly in neurons (reviewed by Serrano-Pozo et al. 2011).

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
0071c7ce83
Confidence
Medium
Networks

PubMed 29196815

Amyloid hypothesis is supported by the fact that progressive Aβ deposition is observed in early, preclinical stages of AD and, finally, in all AD patients.

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
7e050c51dd
Confidence
High
Networks

PubMed 19293145

An increasing ratio of the full-length, 1–42 peptide to the 1–40 form is associated with disease (Kumar-Singh et al., 2006), and mutations underlying familial forms of AD either increase this ratio or increase the amount of Abeta secreted.

BEL
path(MESH:"Alzheimer Disease") association sec(a(CHEBI:"amyloid-beta"))
Hash
7b20c2327a
Networks

PubMed 19293145

APP and APP/presenilin-1 (PS-1) mice do not show neurodegeneration (Irizarry et al., 1997) and yet show several features of AD, including accumulation of plaques and defects in learning (Hsiao et al., 1996), suggesting that many features of AD are not the result of neuronal loss. These animals nonetheless have swollen cholinergic nerve terminals at 12 months, suggesting defective nerve sprouting (Hernandez et al., 2001).

BEL
path(MESH:"Alzheimer Disease") association a(CHEBI:"amyloid-beta")
Hash
5831879c01
Networks

PubMed 25514383

With the progression of the disease the amount of Abeta increases, it starts to accumulate, and becomes toxic for the neurons (Hernandez et al., 2010)

BEL
path(MESH:"Alzheimer Disease") positiveCorrelation a(CHEBI:"amyloid-beta")
Hash
f99ef92040
MeSHDisease
Alzheimer Disease
Networks

PubMed 14556719

Taken together, several lines of evidence point to a reduced UPS function in AD and suggest that both Abeta and tau are important players in the game.

BEL
path(MESH:"Alzheimer Disease") association a(CHEBI:"amyloid-beta")
Hash
e1b4228f3b
Networks

PubMed 29626319

However, their dysfunction in AD due to some factors will reduce Aβ clearance

BEL
path(MESH:"Alzheimer Disease") decreases deg(a(CHEBI:"amyloid-beta"))
Hash
a9b4b1d835
Networks

PubMed 29626319

However, recently, it has been reported that the expression and transport activity of P-gp are impaired in sporadic AD as a result of its ubiquitination, internalization, and proteasome-dependent degradation derived from Aβ40 (Chiu et al. 2015; Hartz et al. 2016), which will result in Aβ deposition

BEL
path(MESH:"Alzheimer Disease") increases a(CHEBI:"amyloid-beta")
Hash
9f69899af6
Networks

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.