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Journal ArticleDOI

The use of real-time PCR analysis in a gene expression study of Alzheimer's disease post-mortem brains.

TLDR
Real-time PCR analysis results indicate that mRNA expression can be detected in all brain specimens for beta-actin, 18S rRNA, GAPDH, and also synaptophysin, a known marker for AD, and suggest that synaptophysical activity is down-regulated in AD brain specimens compared to control brain specimens.
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This article is published in Journal of Neuroscience Methods.The article was published on 2004-01-15. It has received 117 citations till now. The article focuses on the topics: Gene expression & Regulation of gene expression.

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Citations
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Journal ArticleDOI

Impaired Mitochondrial Dynamics and Abnormal Interaction of Amyloid Beta with Mitochondrial Protein Drp1 in Neurons from Patients with Alzheimer’s Disease: Implications for Neuronal Damage

TL;DR: Results from the study suggest that abnormal mitochondrial dynamics increase as AD progresses, and inhibitors of these abnormal interactions may be a therapeutic strategy to reduce mitochondrial fragmentation, neuronal and synaptic damage and cognitive decline in patients with AD.
Journal ArticleDOI

Validation of Zebrafish (Danio rerio) Reference Genes for Quantitative Real‐time RT‐PCR Normalization

TL;DR: The zebrafish GAPDH gene appears unsuitable as reference gene for both types of studies, and the EF1α, Rpl13α and 18S rRNA genes are more suitable as a reference gene panel for zebra fish tissue analysis.
Journal ArticleDOI

Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease

TL;DR: The results revealed an accumulation of intraneuronal oligomeric Aβ, leading to mitochondrial and synaptic deficiencies, and ultimately causing neurodegeneration in AβPP cultures, but found that the mitochondria-targeted antioxidant SS31 restored mitochondrial transport and synaptic viability, and decreased the percentage of defective mitochondria, indicating that SS31 protects mitochondria and synapses from Aβ toxicity.
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Differential expression of oxidative phosphorylation genes in patients with Alzheimer's disease: implications for early mitochondrial dysfunction and oxidative damage.

TL;DR: It is proposed that an increase in cytochrome oxidase gene expression might be the result of functional compensation by the surviving neurons or an early mitochondrial alteration related to increased oxidative damage in AD brains.
References
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Journal ArticleDOI

Neuropathological stageing of Alzheimer-related changes.

Heiko Braak, +1 more
TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.
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Alzheimer's Disease: Genes, Proteins, and Therapy

TL;DR: Evidence that the presenilin proteins, mutations in which cause the most aggressive form of inherited AD, lead to altered intramembranous cleavage of the beta-amyloid precursor protein by the protease called gamma-secretase has spurred progress toward novel therapeutics and provided discrete biochemical targets for drug screening and development.
Journal ArticleDOI

Absolute quantification of mRNA using real-time reverse transcription polymerase chain reaction assays.

TL;DR: The technical aspects involved are discussed, conventional and kinetic RT-PCR methods for quantitating gene expression are contrasted, and the usefulness of these assays are illustrated by demonstrating the significantly different levels of transcription between individuals of the housekeeping gene family, glyceraldehyde-3-phosphate-dehydrogenase (GAPDH).
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Housekeeping genes as internal standards: use and limits.

TL;DR: It is recalled that the commonly used internal standards can quantitatively vary in response to various factors and possible variations are illustrated using three experimental examples.
Journal ArticleDOI

Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease

TL;DR: Levels of synaptotagmin and GAP43 were unchanged in mild AD, but cases with CDR of >1 had a progressive decrement in these synaptic proteins, indicating that synaptic injury in frontal cortex is an early event in AD.
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