Ongoing Work on an Alzheimer's Vaccine
Several different lines of work aim at directing the immune system to remove proteins involved in causing Alzheimer's disease pathology. This is one example:
Since the first case of Alzheimer's was described, the disease has been associated with the presence of insoluble deposits called amyloid plaques. However, in the past decade researchers have been able to conclude that the neuronal death characteristic of the disease is not due to the presence of these plaques but to the toxicity of the soluble aggregates preceding them (and called oligomers).Immunotherapy, consisting of the use of antibodies as a treatment for the disease, is turning out to be a encouraging tool in the treatment of certain types of cancer and has also been used in trials to treat Alzheimer's disease. Nevertheless, the clinical trial which had advanced most in treating Alzheimer's through passive vaccination - using the bapineuzumab antibody - was halted in 2012 during its last trial phase due to the adverse effects of the treatment. Many scientists believe the effects were the result of administering complete antibodies, which produce inflammation in the brain. For this reason, they propose to administer antibody fragments, which has been seen to be much safer.
The research group [thus] designed a recombinant antibody fragment (called scFv-h3D6: single-chain variable Fragment), a derivative of bapineuzumab, which only contains the active part that fights against the etiological agent of the disease: the domains of the antibody responsible for the union of Aβ oligomers. Scientists observed how, in human cell cultures, this antibody fragment protects from cell death and described the molecular mechanism by which this antibody fragment removes the Aβ oligomers that cause the disease.
Mice models of Alzheimer's have been treated successfully with [the] antibody fragment. One abdominal injection and only five days later the animals improved their memory and ability to learn as the result of less aggregated toxins and an increase in the number of neurons. At [the] molecular level, researchers demonstrated two important facts: first, the new treatment eliminates from the cerebral cortex [the] oligomers, the elements causing the disease; and second, that this elimination is linked to the recovery in levels of certain apolipoproteins which are suspected to be the natural eliminators of Aβ peptide aggregations.