The Mitochondrion: A Potential Therapeutic Target for Alzheimer’s Disease

Lu, Mei-Hong; Zhao, Xiu-Yun; Yao, Pei-Pei; Xu, De-En

doi:10.1007/s12264-018-0310-y

Cited by 19 publications

(19 citation statements)

References 33 publications

(44 reference statements)

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“…It is worth noting that accumulated Aβ and hyperphosphorylated tau also contribute to mitochondrial dysfunction in AD brains (Lu et al, 2018). Extracellular Aβ is internalized and imported to the mitochondria via interacting with TOM40 and TIM20, eventually localizing cross mitochondrial membrane (Hansson Petersen et al, 2008).…”

Section: Mitochondrial Dysfunction In Alzheimer’s Diseasementioning

confidence: 99%

“…Accumulation of Aβ or hyperphosphorylated tau causes mitochondrial dysfunction, which in turn execrates Aβ accumulation and tau hyperphosphorylation. The latter cause further damages on mitochondria through multiple mechanisms (Lu et al, 2018). Thus, various strategies that enhancing mitochondrial homeostasis have been used to treat AD in both animal models and clinical trials.…”

Section: Mitochondrial Dysfunction In Alzheimer’s Diseasementioning

confidence: 99%

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Mitochondrial Dysfunction in Neural Injury

Zhao¹,

Lu²,

Yuan³

et al. 2019

Front. Neurosci.

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Mitochondria are the double membrane organelles providing most of the energy for cells. In addition, mitochondria also play essential roles in various cellular biological processes such as calcium signaling, apoptosis, ROS generation, cell growth, and cell cycle. Mitochondrial dysfunction is observed in various neurological disorders which harbor acute and chronic neural injury such as neurodegenerative diseases and ischemia, hypoxia-induced brain injury. In this review, we describe how mitochondrial dysfunction contributes to the pathogenesis of neurological disorders which manifest chronic or acute neural injury.

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Section: Mitochondrial Dysfunction In Alzheimer’s Diseasementioning

confidence: 99%

Section: Mitochondrial Dysfunction In Alzheimer’s Diseasementioning

confidence: 99%

Mitochondrial Dysfunction in Neural Injury

Zhao¹,

Lu²,

Yuan³

et al. 2019

Front. Neurosci.

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“…Acetyl-CoA synthetase (ACS) assay ACS activity was evaluated by measuring the formation of acetyl-hydroxamate (Mart ınezblanco et al, 1992;Lu et al, 2018). The reaction mixture contained MgCl 2 (0.2 M, 12.5 mL), ATP (0.1 M, 50 mL), CoA (20 mM, 30 mL), sodium acetate (0.2 M, 30 mL) and hydroxylamine solution (pH 8.0, 50 mL, prepared by mixing 1 mL of 4 M hydroxylamine hydrochloride and 1 mL of 4 M KOH).…”

Section: Quantification Of Acetyl-coamentioning

confidence: 99%

Functional prediction and characterization of Dip2 gene in mice

Chen

et al. 2019

Cell Biology International

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Disconnected interacting protein 2 (DIP2) is a highly conserved protein family among invertebrates and vertebrates, but its function remains unclear. In this paper, we summarized the conservation of gene sequences and protein domains of DIP2 family members and predicted that they may have a similar functional role in acetyl-coenzyme A (acetyl-CoA) synthesis. We then used the most characterized member, disconnected interacting protein 2 homolog A (DIP2A), for further study. DIP2A is a cytoplasmic protein that is preferentially localized to mitochondria, and its acetyl-CoA synthetase activity has been demonstrated in vitro. Furthermore, the level of acetyl-CoA in HEK293 cells overexpressing DIP2A was increased, which is consistent with its metabolically related function. Together, these data enrich the evolutionary and functional characterization of dip2 genes and provide significant insights into the identification and application of other homologs of DIP2.

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“…In 2004, Swerdlow and Khan [ 4 ] proposed a ‘mitochondrial cascade hypothesis’, which declared that mitochondrial dysfunction results in ATP production decline and excessive reactive oxygen species production, which lead to the formulation of Aβ plaques and neurofibrillary tangles. In return, Aβ and pTau interfered with enzyme metabolism and the dynamic system of mitochondria [ 5 ]. In addition, autophagy dysfunction leads to reducing the clearance of damaged mitochondria and subsequent accumulation in cells, which in return exacerbates mitochondrial damage [ 6 ].…”

Section: Introductionmentioning

confidence: 99%