by Henry Hayter
Alzheimer’s disease is a degenerative neurological disease which is responsible for around 60% of the over 50 million dementia diagnoses world wide. The disease causes the brain tissues to atrophy most commonly in the Hippocampus which plays a large role in learning and memory and the Cerebral cortex which is largely responsible for voluntary movement. The exact causes of the disease are unknown although research has been focused on Tau and Amyloid proteins which are commonly found within neurons. Tau proteins are soluble proteins associated with microtubules in neurons and Amyloid proteins which are suspected to aid in the movement of neurons during brain development. Generally the disease is not considered to be inherited although variants such as early onset Alzheimer’s are suspected to be caused by mutations to the DNA which can be inherited and act as risk factors for the disease.
The causes of Alzheimer’s symptoms are thought to be the tangling of Tau proteins forming neurofibrillary tangles and the buildup of Amyloidβ plaque in the brain which disrupts cell to cell communication. Both causes begin several years before symptoms become apparent making the disease more challenging to treat as often brain atrophy will begin before a diagnosis can be made.
As of now there are no curative or preventative treatments for Alzheimer’s disease available for people. However, recently the University of Leicester along with Göttingen university and LifeArc have begun trials of treatment that has, in mice ,shown to be both curative of Alzheimer’s symptoms and preventative of its development. The treatment involves neutralising the truncated soluble Aβ without involving the regular amyloid protein or the non soluble plaque of Aβ. This is achieved through a humanised antibody originally found in mice which only binds to truncated Aβ called TAP01_04. During the research the Aβ was found to have folded on itself into a hairpin structure which was then used to engineer a stabilised protein in the hairpin shape which the TAP01_04 could bind to. Professor Carr stated that the intention was to trigger an immune response of TAP01_04 antibodies using the engineered protein. When the engineered Aβ was tested in mice TAP01_04 was produced. It was then found that in mice ` Based on similar imaging techniques to those used to diagnose Alzheimer’s in humans, they found that both the antibody and the vaccine helped to restore neuron function, increase glucose metabolism in the brain, restore memory loss and – even though they weren’t directly targeted - reduce amyloid beta plaque formation.`[1] The TAP01_04 and the engineered protein are very different to other treatments in trial due to the fact they target the hair pinned structure and not the regular Aβ. In this way the researchers at Leicester, Göttingen and LifeArc hope that the treatment will prove to be transformative.
The treatment is now looking to be expanded into the early clinical phase of trial.
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