Sökning: "Alzheimer’s disease"

Visar resultat 6 - 10 av 579 avhandlingar innehållade orden Alzheimer’s disease.

1. 6. Cognitive erosion and its implications in Alzheimer’s disease

   Författare :Selina Mårdh; Thomas Karlsson; Anders Wallin; Linköpings universitet; []
   Nyckelord :Alzheimer’s disease; longitudinal study; mixed methods design; semantic memory; awareness; metacognition; central coherence; emotions; Alzheimers sjukdom; longitudinell studie; mixed methods design; semantiskt minne; medvetande; metakognition; central koherens; emotioner; Do Psychology;

   Sammanfattning : The aim of the present thesis was twofold, first to map the semantic memory decline in Alzheimer patients over time, second to take the patient’s perspective and create a multifaceted picture of the individual with Alzheimer’s disease through the study of memory, awareness, central coherence and emotions. Further issues concerned how Alzheimer individuals handled their cognitive erosion in everyday life and if they were well calibrated with their spouse in disease related matters. LÄS MER

3. 7. Genetic Studies of Alzheimer's Disease

   Författare :Elin Blom; Anna Glaser; Martin Ingelsson; Lars Lannfelt; Jan Hillert; Uppsala universitet; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer s disease; Linkage; Affected sib-pairs; APOE; APP duplication; 10q21; 19q13; Wnt signaling; Geriatrics and medical gerontology; Geriatrik och medicinsk gerontologi;

   Sammanfattning : Patients with Alzheimer's disease (AD) often have a family history of the disease, implicating genetics as a major risk factor. Three genes are currently known to cause familial early-onset AD (65 years), only the APOE gene has repeatedly been associated to AD, where the ε4 allele increases disease risk and decreases age at onset. LÄS MER

4. 8. 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

5. 9. Neuroinflammation in Alzheimer’s disease and obesity

   Författare :Linda Tracy; Kerstin Iverfeldt; Colin Combs; Stockholms universitet; []
   Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; NATURVETENSKAP; NATURAL SCIENCES; Alzheimer s disease; obesity; neuroinflammation; neurokemi med molekylär neurobiologi; Neurochemistry with Molecular Neurobiology;

   Sammanfattning : Alzheimer’s disease (AD) and obesity are both major problems in the western world. Although they may appear to have little in common at first glance, they are both characterized by chronic inflammation. Exactly how inflammation affects these disorders is far from clear. LÄS MER

7. 10. 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