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Keywords: Alzheimer's disease (AD)
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Articles

Amyloid β-peptide-dependent activation of human platelets: essential role for Ca 2+ and ADP in aggregation and thrombus formation

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Ilaria Canobbio, Gianni F. Guidetti, Barbara Oliviero, Daria Manganaro, Dina Vara, Mauro Torti, Giordano Pula
Journal: Biochemical Journal
Biochem J (2014) 462 (3): 513–523.
https://doi.org/10.1042/BJ20140307
Published: 22 August 2014
... demonstrate that the amyloid β-peptide activates platelets and that adenosine diphosphate released by platelets plays a critical part in the thrombogenic activity of this molecule. This could be an important component of the cerebrovascular complications of Alzheimer's disease. ADP Alzheimer’s disease...
View articletitled, Amyloid β-peptide-dependent activation of human platelets: essential role for Ca 2+ and ADP in aggregation and thrombus formation
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Includes: Supplementary data
Articles

Kinetics of Torpedo californica acetylcholinesterase inhibition by bisnorcymserine and crystal structure of the complex with its leaving group

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Cecilia Bartolucci, Jure Stojan, Qian-sheng Yu, Nigel H. Greig, Doriano Lamba
Journal: Biochemical Journal
Biochem J (2012) 444 (2): 269–277.
https://doi.org/10.1042/BJ20111675
Published: 11 May 2012
... acetylcholinesterase (AChE) Alzheimer's disease (AD) bisnorcymserine bisnoreseroline carbamate enzyme kinetics X-ray crystal structure The frequency of age-related neurodegenerative disorders and, in particular, of AD (Alzheimers's disease) is expected to greatly rise with the increasing average age...
View articletitled, Kinetics of Torpedo californica acetylcholinesterase inhibition by bisnorcymserine and crystal structure of the complex with its leaving group
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Includes: Supplementary data
Articles

MOCA is an integrator of the neuronal death signals that are activated by familial Alzheimer's disease-related mutants of amyloid β precursor protein and presenilins

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Nobuyuki Tachi, Yuichi Hashimoto, Masaaki Matsuoka
Journal: Biochemical Journal
Biochem J (2012) 442 (2): 413–422.
https://doi.org/10.1042/BJ20100993
Published: 13 February 2012
... and immunoblot analysis with antibodies against GST, PS1, PS2 and FLAG. Alzheimer's disease (AD) amyloid β precursor protein (APP) modifier of cell adhesion (MOCA) neuronal death presenilin (PS) In a previous study using a neuronal cell system in which expression of a gene of interest...
View articletitled, MOCA is an integrator of the neuronal death signals that are activated by familial Alzheimer's disease-related mutants of amyloid β precursor protein and presenilins
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Includes: Supplementary data
Articles

Intracellular copper deficiency increases amyloid-β secretion by diverse mechanisms

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Michael A. Cater, Kelly T. McInnes, Qiao-Xin Li, Irene Volitakis, Sharon La Fontaine, Julian F. B. Mercer, Ashley I. Bush
Journal: Biochemical Journal
Biochem J (2008) 412 (1): 141–152.
https://doi.org/10.1042/BJ20080103
Published: 25 April 2008
.... 1 To whom correspondence should be addressed (email [email protected] ). 11 1 2008 29 1 2008 4 2 2008 4 2 2008 © The Authors Journal compilation © 2008 Biochemical Society 2008 Alzheimer's disease (AD) amyloid amyloid precursor protein (APP) copper Menkes...
View articletitled, Intracellular copper deficiency increases amyloid-β secretion by diverse mechanisms
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Articles

Endosomes and lysosomes play distinct roles in sulfatide-induced neuroblastoma apoptosis: potential mechanisms contributing to abnormal sulfatide metabolism in related neuronal diseases

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Youchun Zeng, Hua Cheng, Xuntian Jiang, Xianlin Han
Journal: Biochemical Journal
Biochem J (2008) 410 (1): 81–92.
https://doi.org/10.1042/BJ20070976
Published: 29 January 2008
... 10 2007 © The Authors Journal compilation © 2008 Biochemical Society 2008 Alzheimer's disease (AD) ceramide electrospray ionization MS (ESI–MS) metachromatic leukodystrophy shotgun lipidomics sulfatide Sulfatides are a class of sulfated GalCers (galactosylceramides...
View articletitled, Endosomes and lysosomes play distinct roles in sulfatide-induced neuroblastoma apoptosis: potential mechanisms contributing to abnormal sulfatide metabolism in related neuronal diseases
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