Search for dissertations about: "APLP2"

Showing result 1 - 5 of 9 swedish dissertations containing the word APLP2.

2. 1. α-Secretase processing of the Alzheimer amyloid-β precursor protein and its homolog APLP2

   Author : Kristin Jacobsen; Kerstin Iverfeldt; Olav Andersen; Stockholms universitet; []
   Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; APP; APLP2; ADAM10; TACE; Alzheimer s Disease; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Abstract : The amyloid-β precursor protein (APP) has been widely studied due to its role in Alzheimer´s disease (AD). When APP is sequentially cleaved by β- and γ-secretase, amyloid-β (Aβ) is formed. Aβ is prone to aggregate and is toxic to neurons. READ MORE

4. 2. Processing of the amyloid precursor protein and its paralogues amyloid precursor-like proteins 1 and 2

   Author : Linda Adlerz; Kerstin Iverfeldt; Richard Cowburn; Stockholms universitet; []
   Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; APP; APLP1; APLP2; Alzheimer s disease; Amyloid β-peptide; Processing; RA; BDNF; IGF-1; curcumin; PI3-K; MAPK; cdk5; Neurochemistry; Neurokemi; Neurochemistry and Molecular Neurobiology; neurokemi med molekylär neurobiologi;

   Abstract : Alzheimer’s disease (AD) is a neurodegenerative disorder which is histopathologically characterised by amyloid plaques and neurofibrillary tangles. Amyloid plaques consist of the amyloid β-peptide (Aβ) that can form aggregates in the brain. Aβ is generated from the amyloid precursor protein (APP) through proteolytic cleavage. READ MORE

5. 3. Proteolytic processing of the Alzheimer APP protein family during neuronal differentiation

   Author : Sofia Holback; Kerstin Iverfeldt; Nigel Hooper; Stockholms universitet; []
   Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; APP; APLP1; APLP2; differentiation; processing; retinoic acid; secretase; Neurochemistry; Neurokemi; Neurochemistry and Molecular Neurobiology; neurokemi med molekylär neurobiologi;

   Abstract : Increased amyloid-β (Aβ) load in the brain, neurite degeneration, neuronal loss, and decreased levels of several neurotrophins are among the characteristics of Alzheimer’s disease (AD). Generation of Aβ occurs when the amyloid precursor protein (APP) is proteolytically processed by β- and γ-secretases in the amyloidogenic pathway. READ MORE

6. 4. Temporal events in neuronal differentiation and cell death : expression and processing of the Alzheimer's amyloid precursor protein family and a protein at the nuclear pore

   Author : Marie Beckman; Kerstin Iverfeldt; David H. Small; Stockholms universitet; []
   Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Neurochemistry; Neurokemi; Neurochemistry and Neurotoxicology; neurokemi och neurotoxikologi;

   Abstract : The present study had two major objectives: 1) to elucidate the involvement of Alzheimer’s amyloid precursor protein (APP) family in neuronal differentiation, and the effect of the Alzheimer’s disease (AD)-linked mutation APPV642I on signal transduction; 2) to investigate the fate of the nuclear pore complex protein POM121 during apoptosis and to examine the possibility of using green fluorescent protein (GFP)-labelled POM121 as a non-invasive sensor of apoptosis in living (non-fixed) cells.APP is the parent protein of the b-amyloid peptide, which is the major peptide constituent in the “senile plaques” of AD. READ MORE

7. 5. Processing of the APP family by the α-secretases ADAM10 and TACE

   Author : Kristin Jacobsen; Kerstin Iverfeldt; Lars Nilsson; Stockholms universitet; []
   Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Neurochemistry; Neurokemi; Neurochemistry and Molecular Neurobiology; neurokemi med molekylär neurobiologi;

   Abstract : Alzheimer’s disease (AD) is a progressive neurodegenerative disease, which is characterized by formation of amyloid plaques in the brain. The major constituent of these plaques is the hydrophobic peptide Aβ. Aβ accumulation is considered to be the main cause of the pathology seen in AD brains. READ MORE