Alzheimer's disease is a neuro-degenerative illness and is the most common form of dementia. At current there are over three quarters of a million suffers in the UK alone. The disease is devastating, not only for those affected, but also their friends and family. The cause of the cognitive impairment is linked to multiple neuron death within the brain. It is thought that the proteins beta-amyloid and tau are responsible for this, and other implications of the disease. Beta-amyloid and tau currently form the basis for most of the current research into the disease.
Beta-amyloid aggregates into clumps within the brain. It forms when the amyloid precursor protein (APP) is cleaved by the enzyme gamma-secretase. It forms a cascade effect whereby the dangerous beta-amyloid peptide is released. There is another enzyme that cleaves APP, it is called alpha-secretase. The beta-amyloid formation drives the pathogenesis of the disease by forming plaques that become harder and harder to clear. Currently scientists are looking at methods of prevention with the beta-amyloid cascade, and have considered methods ranging from inhibition and therapeutic peptides.
Tau inhibits the structure of the neuron through hyper-phosphorylation. This results in the collapse of neuron and lead to neuron death. The tau wraps around the neuron and interferes with synaptic responses. This is what is thought to cause the cognitive impairment as electrical activity as seen in many positron emission tomography scans, is greatly reduced.
Beta-amyloid and tau seem to appear together as without beta-amyloid, there is no tau. Due to this, research could be led to target just beta-amyloid however as there is much debate on this topic, research is being targeted into both the roles of beta-amyloid and tau in Alzheimer's disease. As a result the relationship between these two proteins may be uncovered and provide an answer to the argument; beta-amyloid or tau- which protein is more figurative and how can they be inhibited to provide a biological cure?
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