Alzheimer's vaccine draws closer
22 November, 2018
Building on decades of research, a new paper brings us one step closer to a vaccine that targets the neurological hallmarks of Alzheimer's disease. Prevention may soon be possible.
Alzheimer's disease, the most common form of dementia, is a degenerative neurological disease.
Memory issues are often the first sign of the condition, which steadily progresses over time.
Alzheimer's disease is a growing concern as it appears almost exclusively in older adults. As the number of older people rises in the United States, the number of cases will also increase.
Although scientists are still investigating the exact causes of Alzheimer's disease, they believe that certain neurological markers play a significant role.
The disease seems to involve a buildup of specific proteins in the brain called beta-amyloid and tau. Doctors refer to these abnormal congregations as plaques and neurofibrillary tangles respectively.
The hunt for a vaccine
Current treatments for Alzheimer's do not stop disease progression, so the search for effective alternatives is ongoing. Some researchers hope that targeting amyloid buildup might make it possible to stop Alzheimer's in its tracks.
Many scientists are on the hunt for a vaccine, including Dr. Roger Rosenberg, founding director of the Alzheimer's Disease Center at UT Southwestern in Dallas, TX.
Earlier studies demonstrated that introducing antibodies to amyloid proteins significantly reduces protein buildup. In the early 2000s, scientists used this knowledge to create a vaccine. However, when they tested the vaccine in humans, it caused inflammation in the brains of 6 percent of the participants, making it too dangerous to be usable.
Since then, scientists have focused on developing a way to produce antibodies that bind to Alzheimer's proteins without triggering the T-cell response that led to brain inflammation.
In Dr. Rosenberg's latest paper, he describes a new approach. His team started by injecting DNA coding for amyloid into the skin rather than the muscle. The injected cells created a three-molecule chain of beta-amyloid (ab42).
This molecule chain sparked an immune response, generating antibodies that target ab42. The antibodies prevented the buildup of amyloid plaques and also indirectly prevented the buildup of tau.
The current study examined this response in mice and found that the vaccine produced a 40 percent reduction in beta-amyloid and up to a 50 percent reduction in tau. Importantly, there were no adverse immune reactions.
"This study is the culmination of a decade of research that has repeatedly demonstrated that this vaccine can effectively and safely target in animal models what we think may cause Alzheimer's disease," says Dr. Rosenberg, who is excited about the results. "I believe we're getting close to testing this therapy in people."
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