path(HBP:"mitochondrial dysfunction")

Entity

Name

mitochondrial dysfunction

Namespace

HBP

Namespace Version

20181212

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/56d6631d06deeead416b3b5100d3b4b8d88c29c6/export/hbp-names.belns

Arora et al. (2013) investigated, in a cellular system, the effect of prolonged Abeta exposure on nAChR function. The rodent neuroblastoma cell line NG108-15 was transfected with alpha4beta2 nAChRs and treated for three days with 100 nM Abeta. The following acute stimulation with Abeta and nicotine led to receptor activation that caused a perturbation of intracellular calcium homeostasis followed by mitochondrial dysfunction and increased oxidative stress (Arora et al., 2013) PubMed:25514383

In mechanistic studies, it was proposed that methylene blue inhibits the Aβ-ABAD interaction and decreases mitochondrial dysfunction by decreasing the expression of ABAD levels, in addition to decreasing Aβ levels. PubMed:30444369

Mitochondrial dysfunction is the hallmark of Aβ-induced toxicity. 50-52 PubMed:30444369

Mitochondria are instrumental in the regulation of energy metabolism, and impairment in mitochondrial function has been implicated in the pathogenesis of AD, leading to the mitochondrial cascade hypothesis of AD [121]. PubMed:29758300

Altogether, as with proteinopathy, accumulation of damaged or dysfunctional mitochondria is detrimental to the development of AD pathologies PubMed:29758300

Dysfunctional mitochondria are critically harmful to cells, as this leads to decreased synthesis of cellular ATP and accumulation of ROS, which further overburden and damage other functional mitochondria. PubMed:29758300

Dysfunctional mitochondria are critically harmful to cells, as this leads to decreased synthesis of cellular ATP and accumulation of ROS, which further overburden and damage other functional mitochondria. PubMed:29758300

Previous studies demonstrate impaired mitochondrial function preceding the accumulation of hallmark proteins in AD, such as Aβ [123,124] and tau [125]. PubMed:29758300

Previous studies demonstrate impaired mitochondrial function preceding the accumulation of hallmark proteins in AD, such as Aβ [123,124] and tau [125]. PubMed:29758300

Thus, as a quality control mechanism, mitophagy − a form of selective macroautophagy that specifically targets mitochondria − occurs in response to damaged or dysfunctional mitochondria in order to prevent mitochondrial bioenergetic deficits. PubMed:29758300