Alzheimer's disease, media representations and the politics of euthanasia: constructing risk and selling death in an ageing society

Drawing on extensive data including news media reports and commentaries, documentaries, courts and court reports, films, websites, professional literature and government and non-government agencies, this book explores the 'Alzheimerisation' of the euthanasia debate, examining the shift in recent years in public attitudes towards the desirability and moral permissibility of euthanasia as an end-of-life 'solution' for people living with the disease - not just at its end stage, but also at earlier stages. With attention to mediarepresentations and public understandings of Alzheimer's disease, Alzheimer's Disease, Media Representations and the Politics of Euthanasia sheds light on the processes contributing to these changes in public opinion, investigating the drivers of vexed political debate surrounding the issue and examining the manner in which both sides of the euthanasia debate mobilise support, portray their opponents and make use of media technologies to frame the terms of discourse. Paving the way for a greater level of intellectual honesty with regard to an issue carrying significant policy implications, this book will be of interest to scholars of media and communication, social movements and political communication, and the sociology of health and medicine, as well as researchers and professionals in the fields of palliative and end of life care.

Alzheimer's Abeta fused to green fluorescent protein induces growth stress and a heat shock response

The 42 amino acid Alzheimer's Aβ peptide is involved in the progression of Alzheimer's disease. Here we describe the effects of intracellular Aβ, produced through its attachment to either end of a green fluorescent protein, in yeast. Cells producing Aβ exhibited a lower growth yield and a heat shock response, showing that Aβ fusions promote stress in cells and supporting the notion that intracellular Aβ is a toxic molecule. These studies have relevance in understanding the role of Aβ in the death of neuronal cells, and indicate that yeast may be a new tractable model system for the screening for inhibitors of the stress caused by Aβ.

Nanoformulated mutant SurR9-C84A: a possible key for alzheimer's and its associated inflammation

PURPOSE: Alzheimer's disease (AD) is one of the untreatable neurodegenerative diseases characterised by the pathologic amyloid plaque deposition and inflammation. The aim of this study is to evaluate the neuroprotective effects of nanoformulated SurR9-C84A, a survivin mutant belonging to the inhibitors of the apoptosis (IAP) protein family. The effect of SurR9-C84A was studied against the β-amyloid toxicity and various inflammatory insults in the differentiated SK-N-SH neurons. METHOD: SurR9-C84A loaded poly(lactic-co-glycolic acid) nanoparticles were prepared following the modified double emulsion technique. The neuroprotective effect of SurR9-C84A was evaluated against the amyloid-β (Aβ) peptide fragment, N-methyl-D-aspartate (NMDA) toxicity and the inflammatory assaults. To mimic the in vivo situation, a co-culture of neurons and microglia was also studied to validate these results. RESULTS: SurR9-C84A treatments showed improved neuronal health following Aβ, and NMDA toxicity in addition to inflammatory insults induced in mono and co-cultures. The neuroprotective effect was evident with the reduced neuronal death, accelerated expression of neuronal integrity markers (neurofilaments, beta-tubulin III etc.,) and the neuroprotective ERK/MAPK signalling. CONCLUSION: The current results demonstrated that the SurR9-C84A nanoformulation was very effective in rescuing the neurons and holds a potential future application against AD.