Calcineurin regulates APP metabolism

2021 ◽  
Author(s):  
Suruchi Utreja
Keyword(s):  
App Metabolism

P2-240: The diabetes associated protein, SorCS1 regulates APP metabolism

2011 ◽  
Vol 7 ◽  
pp. S388-S389
Author(s):  
Rachel Lane ◽  
Alan Attie ◽  
Michelle Ehrlich ◽  
Sam Gandy
Keyword(s):  
App Metabolism

P1-213 ADAM10, ADAM17 and BACE1 downregulation in HEK293 cells: effects on APP metabolism

2004 ◽  
Vol 25 ◽  
pp. S156-S157
Author(s):  
Dario Finazzi ◽  
Maura Poli ◽  
Luisa Benerini Gatta
Keyword(s):  
Hek293 Cells ◽  
App Metabolism

scholarly journals P1-090: The effects of Alzheimer's disease associated transferrin variants on APP metabolism

2010 ◽  
Vol 6 ◽  
pp. S200-S200
Author(s):  
Celeste M. Karch ◽  
Amanda Jeng ◽  
Carlos Cruchaga ◽  
John S. Kauwe ◽  
Nicole Renaud ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
App Metabolism

A free radical-generating system regulates APP metabolism/processing

FEBS Letters ◽  
2010 ◽  
Vol 584 (22) ◽  
pp. 4611-4618 ◽  
Author(s):  
María Recuero ◽  
Teresa Muñoz ◽  
Jesús Aldudo ◽  
Marta Subías ◽  
María J. Bullido ◽  
...  
Keyword(s):  
Free Radical ◽  
App Metabolism ◽  
Generating System

Regulation of APP Metabolism by Protein Phosphorylation

1998 ◽  
pp. 133-140
Author(s):  
J. D. Buxbaum ◽  
A. Ikin ◽  
Y. Luo ◽  
J. Naslund ◽  
S. Sabo ◽  
...  
Keyword(s):  
Protein Phosphorylation ◽  
App Metabolism

The Absence of Myelin Basic Protein Reduces Non-Amyloidogenic Processing of Amyloid Precursor Protein

2021 ◽  
Vol 18 ◽  
Author(s):  
Chika Seiwa ◽  
Ichiro Sugiyama ◽  
Makoto Sugawa ◽  
Hiroaki Murase ◽  
Chiaki Kudoh ◽  
...  
Keyword(s):  
Amyloid Precursor Protein ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Amyloid Β Protein ◽  
Pathological Feature ◽  
Novel Therapy ◽  
App Processing ◽  
App Metabolism

Background: The accumulation of amyloid β-protein (Aβ) in the brain is a pathological feature of Alzheimer’s disease (AD). Aβ peptides originate from amyloid precursor protein (APP). APP can be proteolytically cleaved through amyloidogenic or non-amyloidogenic pathways. The molecular effects on APP metabolism / processing may be influenced by myelin and the breakdown of myelin basic protein (MBP) in AD patients and mouse models of AD pathology. Methods: We directly tested whether MBP can alter influence APP processing in MBP-/- mice, known as Shiverer (shi/shi) mice, in which no functional MBP is produced due to gene breakage from the middle of MBP exon II. Results: A significant reduction of the cerebral sAPPα level in Shiverer (shi/shi) mice was found, although the levels of both total APP and sAPPβ remain unchanged. The reduction of sAPPα was considered to be due to the changes in the expression levels of a disintegrin and metalloproteinase-9 (ADAM9) catalysis and non-amyloid genic processing of APP in the absence of MBP because it binds to ADAM9. MBP -/- mice exhibited increased Aβ oligomer production. Conclusion: Together, these findings suggest that in the absence of MBP, there is a marked reduction of non-amyloidogenic APP processing to sAPPα, and targeting myelin of oligodendrocytes may be a novel therapy for the prevention and treatment of AD.

Mechanistic Studies of the Effect of Presenilins 1 and 2 on APP Metabolism

1998 ◽  
pp. 49-58
Author(s):  
D. J. Selkoe ◽  
W. Xia ◽  
J. Zhang ◽  
M. B. Podlisny ◽  
C. A. Lemere ◽  
...  
Keyword(s):  
Mechanistic Studies ◽  
App Metabolism

scholarly journals Future Therapeutic Perspectives into the Alzheimer’s Disease Targeting the Oxidative Stress Hypothesis

Molecules ◽  
2019 ◽  
Vol 24 (23) ◽  
pp. 4410 ◽  
Author(s):  
Jéssika P. Teixeira ◽  
Alexandre A. de Castro ◽  
Flávia V. Soares ◽  
Elaine F. F. da Cunha ◽  
Teodorico C. Ramalho
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Cell ◽  
The Elderly ◽  
Oxygen Species ◽  
Chain Reaction ◽  
Radical Chain ◽  
App Metabolism ◽  
Radical Chain Reaction

Alzheimer’s disease (AD) is a neurodegenerative disease that is usually accompanied by aging, increasingly being the most common cause of dementia in the elderly. This disorder is characterized by the accumulation of beta amyloid plaques (Aβ) resulting from impaired amyloid precursor protein (APP) metabolism, together with the formation of neurofibrillary tangles and tau protein hyperphosphorylation. The exacerbated production of reactive oxygen species (ROS) triggers the process called oxidative stress, which increases neuronal cell abnormalities, most often followed by apoptosis, leading to cognitive dysfunction and dementia. In this context, the development of new therapies for the AD treatment is necessary. Antioxidants, for instance, are promising species for prevention and treatment because they are capable of disrupting the radical chain reaction, reducing the production of ROS. These species have also proven to be adjunctive to conventional treatments making them more effective. In this sense, several recently published works have focused their attention on oxidative stress and antioxidant species. Therefore, this review seeks to show the most relevant findings of these studies.

scholarly journals Wild type TDP-43 induces neuro-inflammation and alters APP metabolism in lentiviral gene transfer models

2012 ◽  
Vol 235 (1) ◽  
pp. 297-305 ◽  
Author(s):  
Alexander M. Herman ◽  
Preeti J. Khandelwal ◽  
G. William Rebeck ◽  
Charbel E.-H. Moussa
Keyword(s):  
Gene Transfer ◽  
Wild Type ◽  
App Metabolism ◽  
Neuro Inflammation ◽  
Transfer Models

scholarly journals Iron Dyshomeostasis Induces Binding of APP to BACE1 for Amyloid Pathology, and Impairs APP/Fpn1 Complex in Microglia: Implication in Pathogenesis of Cerebral Microbleeds

2019 ◽  
Vol 28 (8) ◽  
pp. 1009-1017 ◽  
Author(s):  
Li Gong ◽  
Xiangzhu Tian ◽  
Jing Zhou ◽  
Qiong Dong ◽  
Yan Tan ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Iron Homeostasis ◽  
Small Vessel Disease ◽  
Regulatory Protein ◽  
Vascular Cognitive Impairment ◽  
Cerebral Microbleeds ◽  
Iron Accumulation ◽  
Amyloid Formation ◽  
Amyloid Pathology ◽  
App Metabolism

As a putative marker of cerebral small vessel disease, cerebral microbleeds (CMBs) have been associated with vascular cognitive impairment. Both iron accumulation and amyloid protein precursor (APP) dysregulation are recognized as pathological hallmarks underlying the progression of CMBs, but their cross-talk is not yet understood. In this study, we found a profound increase of amyloid formation with increasing FeCl3 treatment, and a distinct change in APP metabolism and expression of iron homeostasis proteins (ferritin, Fpn1, iron regulatory protein) was observed at the 300 uM concentration of FeCl3. Further results revealed that extracellular iron accumulation might potentially induce binding of APP to BACE1 for amyloid formation and decrease the capability of APP/Fpn1 in mediating iron export. Our findings in this study, reflecting a probable relationship between iron dyshomeostasis and amyloid pathology, may help shed light on the underlying pathogenesis of CMBs in vascular cognitive impairment.

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