Sökning: "Fe65"

Visar resultat 1 - 5 av 8 avhandlingar innehållade ordet Fe65.

1. 1. The amyloid-β precursor protein (APP) and its adaptor protein Fe65 : Two key players in Alzheimer’s disease

   Författare :Preeti Menon; Anna-Lena Ström; Thorsten Müller; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer s disease; APP; Fe65; Meprinβ; α-secretase; APP processing; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the abnormal accumulation and aggregation of amyloid beta (Aβ) peptides within the brain. Generation of Aβ occur when the amyloid-beta precursor protein (APP) is proteolytically processed by β- and then γ-secretase in the amyloidogenic pathway. LÄS MER

3. 2. Phosphorylation regulates APP and Fe65, two key players in Alzheimer’s disease

   Författare :Preeti Menon; Anna-Lena Ström; Lennart Brodin; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; Alzheimer s disease; APP; Fe65; phosphorylation; RIP; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : Alzheimer’s disease (AD) is a slow progressive neurodegenerative disease characterized by the accumulation of toxic amyloid beta (Aβ) peptide within the brain. APP plays an important role in AD, as the Aβ is formed when APP is sequentially cleaved by β- and γ-secretase. This is known as amyloidogenic processing of APP. LÄS MER

4. 3. The amyloid-β precursor protein (APP)-binding protein Fe65 and APP processing

   Författare :Niina Koistinen; Anna-Lena Ström; Stefan Kins; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; APP; Fe65; ADAM10; Alzheimer s disease; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by abnormal deposition of neurotoxic amyloid-β (Aβ) peptide. Aβ is generated by sequential cleavage of the amyloid-β precursor protein (APP) by β- and then γ-secretase. LÄS MER

5. 4. Links between plasma apoE and glucose metabolism, brain insulin signaling, and synaptic integrity : Relevance to Alzheimer’s disease pathophysiology

   Författare :Anna Edlund; Henrietta Nielsen; William Rebeck; Stockholms universitet; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer’s disease; apolipoprotein E; insulin; metabolism; Amyloid precursor protein APP ; Fe65; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : Human apolipoprotein E (apoE) exists as three main isoforms called apoE2, apoE3, and apoE4, of which the E4 isoform is associated with increased Alzheimer’s disease (AD) risk. Brain glucose hypometabolism, linked to synaptic dysfunction, occurs years before symptom onset in AD, especially in APOEε4-carriers. LÄS MER

7. 5. The adaptor protein Fe65 and APP processing

   Författare :Niina Koistinen; Kerstin Iverfeldt; Susanne Frykman; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : The amyloid precursor protein (APP) protein has been in the limelight of research on Alzheimer´s disease (AD) pathogenesis because its proteolytic processing gives rise to the neurotoxic amyloid β (Aβ) peptide, the main constituent of amyloid plaques in the brains of AD patients. APP is sequentially processed by at least three different proteases termed α-, β-, and γ-secretases. LÄS MER