Alzheimer’s disease (AD) is the most common form of dementia, thought to affect approximately 50 million people worldwide. Despite its prevalence, the actual cause of and mechanisms behind AD symptoms – progressive loss of cognitive function caused by neuron and synapse loss – remain surprisingly elusive.
AD has been identified as a proteopathy, or protein misfolding disease. The most widely held hypothesis for the origin of AD symptoms is that they are caused by an accumulation and aggregation of amyloid beta (Aβ) in the brain; AD symptoms are caused by the breakdown of the cytoskeleton, leading to cell death, and mechanisms have been proposed that link Aβ to this process.
Aβ is a small peptide generated from the proteolytic cleavage of the transmembrane protein amyloid-beta precursor protein (APP) by beta secretase and gamma secretase. Aβ monomers can aggregate to form oligomers, which further aggregate to form protofibrils. These undergo a significant conformational change to form insoluble, beta sheet-dominated fibrils and finally senile plaques that deposit outside neurons.
As well as Aβ, tau, another misfolding protein, is also associated with the development of AD symptoms. Tau normally acts to stabilize the cytoskeleton, but aggregates when hyperphosphorylated to form paired helical filaments and subsequently neurofibrillary tangles. When aggregated, tau’s protective effect on the cytoskeleton disappears, leading to cytoskeleton breakdown. Neuroinflammation is also thought to be central to disease development, explored further in our poster. The overall AD cascade is very complex, especially as many research questions remain unanswered.
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