Mitochondrial abnormalities in Alzheimer brain: Mechanistic implications

By P. Bubber, V. Haroutunian, G. Fisch, J. Blass, G. Gibson. Annals of Neurology, 2005

600 citations recorded by the source corpus.

Subfields: Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/325501ec64c7e52691b7aa83f94cf9ec9b8d9162

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In Biochemistry

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Citations in the corpus

• Oxidative Stress and Mitochondrial Dysfunction in Alzheimer’s Disease (2013, unknown): “Indeed, several key enzymes of oxidative metabolism including α-ketoglutarate dehydrogenase complex, pyruvate dehydrogenase complex, and cytochrome oxidase all demonstrated reduced expression and/or activity in AD [84, 89–94], alteration of which significantly correlated with clinical state and plaq”
• Identification of miRNA Changes in Alzheimer's Disease Brain and CSF Yields Putative Biomarkers and Insights into Disease Pathways (2008, unknown): “In addition, our finding that IDH2 can be regulated by miR-423 and miR-98 agrees with reports that isocitrate dehydrogenase enzyme activity is decreased in AD prefrontal cortex and suggests a mechanism for the relative sparing of the cerebellum [8].”
• Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, background): “Notably, whereas defects in mitochondrial function are a prominent early event in AD (Blass et al., 2000; Swerdlow and Kish, 2002; Zhu et al., 2004; Bubber et al., 2005), whether and how mitochondrial defects contribute to synaptic dysfunction in AD neurons is unclear.”
• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “Bubber et al. (2005) tested impairments in the Krebs cycle enzymes of mitochondria in AD patients and found significantly decreased PDHC and KGDHC activities while the activities of the other four Krebs cycle enzymes were unchanged.”
• The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “They were significantly correlated with the clinical severity and the senile plaque [83].”
• Upregulated function of mitochondria-associated ER membranes in Alzheimer disease (2012, unknown): “…oxidative energy metabolism, calcium buffering capacity, and free radical production; Peterson and Goldman, 1986; Hirai et al , 2001; Gibson and Huang, 2004; Bubber et al , 2005), and thus may be the underlying cause of the reported aberrant mitochondrial phenotypes seen in AD (Su et al , 2010).”
• The amyloid β-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae (2008, background): “It is noteworthy that in AD at an early stage there is already a reduction in the number of mitochondria (14), the brain glucose metabolism is decreased (15), and the activities of both tricarboxylic acid cycle enzymes (16) and cytochrome c oxidase (COX) are reduced (17–20).”
• Mitochondrial Dysfunction in Neurodegenerative Diseases (2012, background): “Activities of the three key tricarboxylic acid cycle enzyme complexes , pyruvate dehydrogenase, isocitrate dehydrogenase, and ␣-ketoglutarate dehydrogenase, are impaired in postmortem AD brain and fibroblasts from patients with AD (Bubber et al., 2005).”
• A construct with fluorescent indicators for conditional expression of miRNA (2008, unknown): “Dysfunction of KGDHC has been observed in the brains of Alzheimer's disease and could cause metabolic deficiency that is associated with the disease [30-35].”