Giovanna mallucci biography sampler
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At Alzheimer’s Research UK, we’re committed to funding the most innovative grass-roots research and translating promising discoveries into benefits for people with dementia as quickly as possible. At the Alzheimer’s Research UK Conference 2016 in Manchester this week we’ve been hearing about some of the latest emerging research from across the UK.
Where are we now?
We read headlines almost every day about potential new drugs on the horizon for diseases like Alzheimer’s but sadly no new drug treatments have been licenced for the disease since 2002. Much recent attention has been focused on drugs that target one of the hallmark Alzheimer’s proteins in the brain called amyloid.
Dr Mike O’Neill from the pharmaceutical company Eli Lilly presented an overview of current drug development approaches. In recent years several clinical trials of drugs against the amyloid protein have sadly not made it to treatments in people’s hands. It’s important we learn from these trials to help shape better approaches to test future treatments.
Dr O’Neill told the room that one of the most important things researchers need in order to test new drugs in the most robust way, is better methods to track the disease they’re trying to treat. The final stages of clinical trials (called phase III trials
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Abstract
The unfolded protein response (UPR) is rapidly gaining momentum as a therapeutic target for protein misfolding neurodegenerative diseases, in which its overactivation results in sustained translational repression leading to synapse loss and neurodegeneration. In mouse models of these disorders, from Alzheimer’s to prion disease, modulation of the pathway—including by the licensed drug, trazodone—restores global protein synthesis rates with profound neuroprotective effects. However, the precise nature of the translational impairment, in particular the specific proteins affected in disease, and their response to therapeutic UPR modulation are poorly understood. We used non-canonical amino acid tagging (NCAT) to measure de novo protein synthesis in the brains of prion-diseased mice with and without trazodone treatment, in both whole hippocampus and cell-specifically.
During disease the predominant nascent proteome changes occur in synaptic, cytoskeletal and mitochondrial proteins in both hippocampal neurons and astrocytes. Remarkably, trazodone treatment for just 2 weeks largely restored the whole disease nascent proteome in the hippocampus to that of healthy, uninfected mice, predominantly with recovery of proteins involved in synaptic and mitochondrial function. In