Reduced platelet amyloid precursor protein ratio (APP ratio) predicts conversion from mild cognitive impairment to Alzheimer’s disease

2012 ◽  
Vol 119 (7) ◽  
pp. 815-819 ◽  
Author(s):  
Isis A. Zainaghi ◽  
Leda L. Talib ◽  
Breno S. Diniz ◽  
Wagner F. Gattaz ◽  
Orestes V. Forlenza
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Protein Ratio ◽  
App Ratio

Transgenic mouse models of Alzheimer's disease: phenotype and mechanisms of pathogenesis

2001 ◽  
Vol 67 ◽  
pp. 195-202 ◽  
Author(s):  
Karen Duff
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Transgenic Mice ◽  
Amyloid Precursor Protein ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Precursor Protein ◽  
Transgenic Mouse Models ◽  
Disease Phenotype

A range of transgenic mice have been created to model Alzheimer's disease. These include mice expressing human forms of the amyloid precursor protein, the presenilins and, more recently, tau. Several of the models develop features of the disease including amyloid pathology, cholinergic deficits, neurodegeneration and cognitive impairment. Progress in the characterization and use of these model animals is discussed.

scholarly journals Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy

Brain ◽  
2019 ◽  
Vol 143 (1) ◽  
pp. 191-209 ◽  
Author(s):  
Sarah Gourmaud ◽  
Haochang Shou ◽  
David J Irwin ◽  
Kimberly Sansalone ◽  
Leah M Jacobs ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Temporal Lobe Epilepsy ◽  
Amyloid Precursor Protein ◽  
Temporal Lobe ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Drug Resistant ◽  
Stress Kinases

Abstract Temporal lobe epilepsy represents a major cause of drug-resistant epilepsy. Cognitive impairment is a frequent comorbidity, but the mechanisms are not fully elucidated. We hypothesized that the cognitive impairment in drug-resistant temporal lobe epilepsy could be due to perturbations of amyloid and tau signalling pathways related to activation of stress kinases, similar to those observed in Alzheimer’s disease. We examined these pathways, as well as amyloid-β and tau pathologies in the hippocampus and temporal lobe cortex of drug-resistant temporal lobe epilepsy patients who underwent temporal lobe resection (n = 19), in comparison with age- and region-matched samples from neurologically normal autopsy cases (n = 22). Post-mortem temporal cortex samples from Alzheimer’s disease patients (n = 9) were used as positive controls to validate many of the neurodegeneration-related antibodies. Western blot and immunohistochemical analysis of tissue from temporal lobe epilepsy cases revealed increased phosphorylation of full-length amyloid precursor protein and its associated neurotoxic cleavage product amyloid-β*56. Pathological phosphorylation of two distinct tau species was also increased in both regions, but increases in amyloid-β1-42 peptide, the main component of amyloid plaques, were restricted to the hippocampus. Furthermore, several major stress kinases involved in the development of Alzheimer’s disease pathology were significantly activated in temporal lobe epilepsy brain samples, including the c-Jun N-terminal kinase and the protein kinase R-like endoplasmic reticulum kinase. In temporal lobe epilepsy cases, hippocampal levels of phosphorylated amyloid precursor protein, its pro-amyloidogenic processing enzyme beta-site amyloid precursor protein cleaving enzyme 1, and both total and hyperphosphorylated tau expression, correlated with impaired preoperative executive function. Our study suggests that neurodegenerative and stress-related processes common to those observed in Alzheimer’s disease may contribute to cognitive impairment in drug-resistant temporal lobe epilepsy. In particular, we identified several stress pathways that may represent potential novel therapeutic targets.

The platelet amyloid precursor protein ratio as a diagnostic marker for Alzheimer’s disease in Thai patients

2013 ◽  
Vol 20 (5) ◽  
pp. 644-648 ◽  
Author(s):  
Chatchawan Srisawat ◽  
Sarawut Junnu ◽  
Chayanon Peerapittayamongkol ◽  
Aree Futrakul ◽  
Rungtip Soi-ampornkul ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Diagnostic Marker ◽  
Precursor Protein ◽  
Protein Ratio

scholarly journals Alteredβ-Amyloid Precursor Protein Isoforms in Mexican Alzheimer’s Disease Patients

2006 ◽  
Vol 22 (3) ◽  
pp. 119-125 ◽  
Author(s):  
V. J. Sánchez-González ◽  
G. G. Ortiz ◽  
P. Gallegos-Arreola ◽  
M. A. Macías-Islas ◽  
E. D. Arias-Merino ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Amyloid Precursor Protein ◽  
Precursor Protein ◽  
Protein Isoforms ◽  
Control Subjects ◽  
High Risk Factor ◽  
Healthy Control ◽  
App Ratio

Objective: To determine theβ-amyloid precursor protein (βAPP) isoforms ratio as a risk factor for Alzheimer’s Disease and to assess its relationship with demographic and genetic variables of the disease.Methods: Blood samples from 26 patients fulfilling NINCDS-ADRDA diagnostic criteria for AD and 46 healthy control subjects were collected for Western blotting forβAPP. A ratio ofβAPP isoforms, in optical densities, between the upper band (130 Kd) and the lower bands (106–110 Kd) was obtained. Odds ratios were obtained to determine risk factor of this component.Results:βAPP ratio on AD subjects was lower than that of control subjects: 0.3662 ± 0.1891 vs. 0.6769 ± 0.1021 (mean ± SD, p<0.05). A lowβAPP ratio (<0.6) showed an OR of 4.63 (95% CI 1.45 ± 15.33). When onset of disease was taken into account, aβAPP ratio on EOAD subjects of 0.3965 ± 0.1916 was found vs. 0.3445 ± 0.1965 on LOAD subjects (p>0.05).Conclusions: AlteredβAPP isoforms is a high risk factor for Alzheimer’s disease, although it has no influence on the time of onset of the disease.

Memapsin 2, a drug target for Alzheimer's disease

2003 ◽  
Vol 70 ◽  
pp. 213-220 ◽  
Author(s):  
Gerald Koelsch ◽  
Robert T. Turner ◽  
Lin Hong ◽  
Arun K. Ghosh ◽  
Jordan Tang
Keyword(s):  
Crystal Structure ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transition State ◽  
Amyloid Precursor Protein ◽  
Therapeutic Target ◽  
Drug Target ◽  
Aspartic Protease ◽  
Precursor Protein ◽  
Memapsin 2

Mempasin 2, a ϐ-secretase, is the membrane-anchored aspartic protease that initiates the cleavage of amyloid precursor protein leading to the production of ϐ-amyloid and the onset of Alzheimer's disease. Thus memapsin 2 is a major therapeutic target for the development of inhibitor drugs for the disease. Many biochemical tools, such as the specificity and crystal structure, have been established and have led to the design of potent and relatively small transition-state inhibitors. Although developing a clinically viable mempasin 2 inhibitor remains challenging, progress to date renders hope that memapsin 2 inhibitors may ultimately be useful for therapeutic reduction of ϐ-amyloid.

Are visual cues helpful for virtual spatial navigation and spatial memory in patients with mild cognitive impairment or Alzheimer’s disease?

2018 ◽  
Vol 32 (4) ◽  
pp. 385-400 ◽  
Author(s):  
Mélanie Cogné ◽  
Sophie Auriacombe ◽  
Louise Vasa ◽  
François Tison ◽  
Evelyne Klinger ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Spatial Memory ◽  
Visual Cues ◽  
Spatial Navigation ◽  
Navigation And Spatial Memory
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