a(HBP:HBP00074)
An exponential increase of brain levels of AβOs in aging mice was observed. PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
Furthermore, the authors demonstrated significant, negative correlation of AβO number with the MMSE scores, what indicates that sFIDA readout seems to reflect the severity of AD, similar to the results described above. PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
In very early stages of AD pathology, before the appearance of amyloid plaques, oligomers assemble perisomatically, rather than intracellularly, surrounding individual diffuse neurons. PubMed:29196815
They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815
The levels of HMW AβOs in AD or MCI patients were significantly higher than in normal controls and correlated inversely with MMSE score. PubMed:29196815
They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815
Moreover, it was postulated that AβOs may trigger a harmful cascade damaging neurons and synapses (Morris et al. 2014). PubMed:29196815
Soluble Aβ oligomers may cause a highly selective neuronal death accelerated by increasing exposure to AβOs (Lambert et al. 1998). PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
Moreover, it was postulated that AβOs may trigger a harmful cascade damaging neurons and synapses (Morris et al. 2014). PubMed:29196815
In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815
These results are in line with findings of Koffie et al. (2009), who revealed that AβOs surrounding plaques contribute to synapse loss in a mouse model of AD. PubMed:29196815
It was also demonstrated that fibril-free AβO solutions are essential for memory loss (Brito-Moreira et al. 2017), while the fibrillar Aβ in amyloid deposits is not the active factor affecting the cognition (Martins et al. 2008). PubMed:29196815
It was also shown that soluble AβOs may directly trigger dysfunction of neural signaling, which leads to early memory loss and the progression of dementia in AD. PubMed:29196815
In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815
In very early stages of AD pathology, before the appearance of amyloid plaques, oligomers assemble perisomatically, rather than intracellularly, surrounding individual diffuse neurons. PubMed:29196815
They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815
It was also shown that soluble AβOs may directly trigger dysfunction of neural signaling, which leads to early memory loss and the progression of dementia in AD. PubMed:29196815
It was also shown that soluble AβOs may directly trigger dysfunction of neural signaling, which leads to early memory loss and the progression of dementia in AD. PubMed:29196815
Moreover, in brain slices, AβOs rapidly inhibited long-term potentiation (LTP) of synapses (Klein et al. 2001). PubMed:29196815
In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815
In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815
In normal rats, impaired memory of a learned behavior was observed after intraventricular application of soluble oligomers of Aβ42 isolated directly from human AD brains (Shankar et al. 2008). Furthermore, AβO injections resulted in reduction of a synapse number and their function in dose-dependent manner. It also led to the inhibition of LTP and enhancement of long-term synaptic depression (LTD) in rodent hippocampus (Shankar et al. 2008). PubMed:29196815
AβOs can trigger changes in Tau protein characteristic for AD (Shankar et al. 2008). They induce hyperphosphorylation of Tau at AD-specific epitopes and cause neuritic dystrophy in cultured neurons. PubMed:29196815
AβOs can trigger changes in Tau protein characteristic for AD (Shankar et al. 2008). They induce hyperphosphorylation of Tau at AD-specific epitopes and cause neuritic dystrophy in cultured neurons. PubMed:29196815
Furthermore, it was demonstrated that AβO may not only injure the neurites of brain neurons, but also activate microglia and astrocyte response (Sondag et al. 2009). PubMed:29196815
Furthermore, it was demonstrated that AβO may not only injure the neurites of brain neurons, but also activate microglia and astrocyte response (Sondag et al. 2009). PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815
Excessive activation of NMDAR by soluble AβOs triggers disproportionate influx of Ca2+ into neurons, which leads to excitotoxicity, mitochondrial dysfunction, and loss of synapses (Zhao et al. 2004). PubMed:29196815
Soluble AβOs, but not monomers, mediate the internalization of the GluA1/GluA2 subunits by endocytosis (Zhang et al. 2011), leading to synaptic dysfunction (Hsieh et al. 2006). PubMed:29196815
Soluble AβOs, but not monomers, mediate the internalization of the GluA1/GluA2 subunits by endocytosis (Zhang et al. 2011), leading to synaptic dysfunction (Hsieh et al. 2006). PubMed:29196815
Synapse targeting of AβOs involves activation of p75NTR. PubMed:29196815
In cultures of mature hippocampal neurons, soluble AβOs caused a rapid, substantial loss of surface IRs, especially on dendrites (Zhao et al. 2010). PubMed:29196815
Furthermore, the authors demonstrated significant, negative correlation of AβO number with the MMSE scores, what indicates that sFIDA readout seems to reflect the severity of AD, similar to the results described above. PubMed:29196815
The levels of HMW AβOs in AD or MCI patients were significantly higher than in normal controls and correlated inversely with MMSE score. PubMed:29196815
They revealed increases in AβOs and soluble TNF-R plasma levels that accurately differentiated mild AD patients from control subjects and to some extent from amnestic mild cognitive impairment (aMCI) patients. PubMed:29196815
It has been postulated that soluble or small oligomeric forms of Ab have deleterious effects in the brain, inducing impaired synaptic function and promoting neuronal degeneration [5]. PubMed:21718217
It has been postulated that soluble or small oligomeric forms of Ab have deleterious effects in the brain, inducing impaired synaptic function and promoting neuronal degeneration [5]. PubMed:21718217
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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.