Search for dissertations about: "prion disease"

Showing result 1 - 5 of 36 swedish dissertations containing the words prion disease.

  2. 1. Structural investigation of SOD1 aggregates in ALS : identification of prion strains using anti-peptide antibodies

    Author : Johan Bergh; Thomas Brännström; Stefan L. Marklund; Peter M. Andersen; Joakim Bergström; Umeå universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; ALS; SOD1; prion; motor neuron disease; neurodegeneration; strain; seeding; protein aggregation; transgenic mice; peptide antibodies; Neurology; neurologi;

    Abstract : Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative syndrome characterized by progressive degeneration of motor neurons that result in muscle wasting. The symptoms advance gradually to paralysis and eventually death. Most patients suffer from sporadic ALS (sALS) but 10% report a familial predisposition. READ MORE

  4. 2. SOD1 prions transmit templated aggregation and fatal ALS-like disease

    Author : Elaheh Ekhtiari Bidhendi; Thomas Brännström; Stefan L. Marklund; Peter M. Andersen; Inger Nennesmo; Umeå universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; ALS; amyotrophic lateral sclerosis; SOD1; prion; neurodegeneration; strain; seeding; protein misfolding; protein aggregation; propagation; transgenic mice; Pathology; patologi; Neurology; neurologi;

    Abstract : Amyotrophic lateral sclerosis (ALS) is an adult-onset fatal neurodegenerative disease characterized by a progressive degeneration of the upper and lower motor neurons. The resulting paresis begins focally, usually in one muscle, and spreads contiguously, leading to muscle wasting, progressive paralysis and eventually death. READ MORE

  5. 3. Novel endogenous mechanisms of complement regulation - A delicate balance

    Author : Andreas Holmér; Malmö Klinisk kemi; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; short leucine rich glycoprotein; factor H; C1q; age-related macular degeneration; C4b-binding protein; prion disease; prion protein; Complement regulation; C-reactive protein;

    Abstract : In this thesis, the biochemical mechanisms for complement activation by endogenous proteins are explored. The short leucine-rich repeat proteins (SLRPs) help organise extracellular matrices. We found that several SLRPs bind C1q and of these, fibromodulin and osteoadherin trigger complement. READ MORE

  6. 4. Protein Folding Activity of the Ribosome and Its Implication in Prion Processes

    Author : Yanhong Pang; Suparna Sanyal; Patricia L. Clark; Uppsala universitet; []
    Keywords : NATURVETENSKAP; NATURAL SCIENCES; Ribosome; Protein folding; Prion disease; Antiprion drug; Competitive inhibition; PFAR; Amyloid; Biology with specialization in Molecular Biology; Biologi med inriktning mot molekylärbiologi;

    Abstract : How the linear protein chains fold into their three-dimensional active conformation is one of the remaining puzzles of modern science. Other than molecular chaperones, ribosome - the cellular protein synthesis machinery, has also been implicated in protein folding. READ MORE

  7. 5. Neuroinflammation and amyloid-β in early Alzheimer’s disease. Insight into the earliest events using mouse models

    Author : Megg Gonzales Garcia; Neuroinflammation; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Alzheimer s disease; amyloid-beta; neuroinflammation; microglia; synapses; prion-like;

    Abstract : Alzheimer’s disease (AD) is the leading cause of dementia and most common neurodegenerative disease worldwide, but there currently exists no effective treatment that can stop nor slow the progression of the disease. The current dogma in the field postulates that the appearance of extracellular amyloid-beta (Aβ) plaques, a histopathological hallmark of the disease, is the trigger for downstream, detrimental events, including neuronal loss, extensive neuroinflammation and cognitive decline. READ MORE