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Neuroscience of Degeneration: Alzeimer's

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 Alzeimer's Disease

Over a century ago a german doctor, Alois Alzeimer spotted anamolies in brain section of patient with dementia. Ever since people have been studying the plaques and tangles that he saw in the hope that one day we could understand and cure what is now known as the Alzeimer's Disease (AD) which is most common Neurodegenerative disease.

Plaques are insoluble peptide called Amyloid beta (A-beta) which are formed when Amyloid Precursor Protein are cleaved by certain enzymes. Abeta is considered as the main culprit for AD. Abeta tends to misfold and sticky eventually clumping together to form oligomers. Some of which aggregate into large insoluble fibrils that deposit in the brain as plaques. Oligomers can be toxic, research shows they can weaken communication and plasticity at synapse. This could be what stops brain from forming or retrieving memories.

Frontiers in Behavioral Neuroscience

Neuron's aren't the only cells affected in AD, astrocytes and microglia also play a role. Microglia are immune cells that clear up waste. Microglia takes up Abeta but they also gets activated by it, triggering the release of inflammatory cytokines that can damage neurons. Microglia also start to remove synapse by using phagocytosis. As synapses start to disappear and neurons die, abnormal brain activity emerge and brain can't process and store the information properly. 

Another key feature of AD is neurodegeneration. Neuronal damage and death is triggered by Abeta but some of Abeta's effects seem to be mediated by another protein seen in the brain of patients: Tau, a component of tangles. Molecules are carried in axon on a series of tracks made of microtubules which are inturn stabilised by Tau. In AD tau is modified causing it to dissociate from microtubul, adopt abnormal shape. These either remain soluble or form aggregate and eventually these process kills the neuron. These misfloded tau protein travels across synapses into a healthy neuron when they make healthy tau protein start to misfold as well spreading pathalogy. The spreading of pathalogy through the brain matches the symptoms of different stages of AD. 

Despite these advanced knowledge and understanding of AD, no cure exists. While drugs are being developed to target Abeta and Tau,it's unclear whether they will be successful in treating the disease. We hope basic and clinical research will one day diagnose and treat this devastating disorder. 

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