Expression of APP pathway mRNAs and proteins in Alzheimer’s disease

@article{Matsui2007ExpressionOA,
  title={Expression of APP pathway mRNAs and proteins in Alzheimer’s disease},
  author={Toshifumi Matsui and Martin Ingelsson and Hiroaki Fukumoto and Karunya Ramasamy and Hisatomo Kowa and Matthew P. Frosch and Michael C. Irizarry and Bradley T. Hyman},
  journal={Brain Research},
  year={2007},
  volume={1161},
  pages={116-123}
}
Amyloid precursor protein glycosylation is altered in the brain of patients with Alzheimer’s disease
TLDR
The analysis of the lectin binding to sAPPα and sAPPβ suggests that glycosylation dictates the proteolytic pathway for APP processing, which may influence the generation of the different APP fragments and, consequently, the pathological progression of AD.
Development and validation of cellular models for studying amyloid precursor protein isoforms.
TLDR
It is suggested that serum in culture medium has no effect on cell number, APP secretion and APP gene expression between isoforms while energy deprivation using 2DG affected cellNumber, APP genes expression and APP production significantly, which confirms the importance of glucose as a source of energy.
Platelet Amyloid Precursor Protein Isoform Expression in Alzheimer's Disease: Evidence for Peripheral Marker
TLDR
The present results are consistent with the hypothesis that platelet APP could be considered a potential reliable peripheral marker for studying AD and could contribute to define a signature for the presence of AD pathology.
Opposite Dysregulation of Fragile-X Mental Retardation Protein and Heteronuclear Ribonucleoprotein C Protein Associates with Enhanced APP Translation in Alzheimer Disease
TLDR
It is shown that, as expected, human APP is overexpressed in hippocampal total extract from Tg2576 mice at all age points, and expression of FMRP and hnRNP C are decreased and increased in hippocampusal synaptosomes from sporadic AD patients.
Amyloid Precursor Protein Revisited
TLDR
APP is a neuron-specific protein under basal and neuroinflammatory conditions, and soluble APP is highly stable in the central nervous system (CNS) and do not undergo further cleavage with or without trophic factor support.
Regulation of the metabolism of the Alzheimer's amyloid precursor protein by contactin 5 and BIN1
TLDR
BIN1 levels were shown to be reduced in the brain during aging and in AD, leading to the hypothesis that more APP is trafficked into the amyloidogenic pathway rather than being degraded, resulting in more Aβ generation so increasing the risk of developing AD.
The amyloid precursor protein: a converging point in Alzheimer's disease.
TLDR
It is argued that the reduction of APP, which would result in a concurrent decrease in Aβ as well as all other toxic APP metabolites, would alleviate the toxic environment associated with AD and slow disease progression.
Intracellular Calcium Dysregulation by the Alzheimer’s Disease-Linked Protein Presenilin 2
TLDR
This contribution focuses on PS2, summarizing how AD-linked PS2 mutants alter multiple Ca2+ pathways and the functional consequences of thisCa2+ dysregulation in AD pathogenesis.
...
...

References

SHOWING 1-10 OF 48 REFERENCES
Amyloid precursor protein mRNA levels in Alzheimer's disease brain.
Relative Increase in Alzheimer’s Disease of Soluble Forms of Cerebral Aβ Amyloid Protein Precursor Containing the Kunitz Protease Inhibitory Domain*
TLDR
An imbalance of isoforms as one possible mechanism for amyloid deposition in sporadic AD is supported, and KPI-containing species of APP may be more amyloidsogenic.
Promoter mutations that increase amyloid precursor-protein expression are associated with Alzheimer disease.
TLDR
Evidence is provided that APP-promoter mutations that significantly increase APP expression levels are associated with Alzheimer disease (AD).
LDL receptor‐related protein (LRP) in Alzheimer's disease: Towards a unified theory of pathogenesis
TLDR
A review of the current knowledge of LRP in AD and its relationship to the other known AD susceptibility markers finds that over‐expression of presenilin 1 results in decreased expression of L RP.
APP with Kunitz type protease inhibitor domain (KPI) correlates with neuritic plaque density but not with cortical synaptophysin immunoreactivity in Alzheimer's disease and non-demented aged subjects: a multifactorial analysis.
TLDR
Findings support previous findings indicating that KPI-APP is an important local factor for amyloid deposition in the neuritic plaques, both in AD and in non-demented aged people.
...
...