A vaccine against Alzheimer’s has come a step closer to reality after scientists succeeded in preventing the build-up of toxic brain proteins linked to the disease.
Experiments on mice showed that the DNA vaccine, injected into skin, could potentially delay the onset of Alzheimer’s with no serious side-effects.
The findings, published in the journal Alzheimer’s Research And Therapy, could pave the way for clinical trials with human patients, said the scientists.
Two kinds of toxic protein or protein building blocks are thought to play a key role in Alzheimer’s – beta-amyloid and tau.
Beta-amyloid accumulates in sticky clumps in the brain and is a characteristic hallmark of the disease seen in patient post-mortem examinations.
Tau is a protein which produces destructive “tangles” within nerve cells. Some research suggests that the two are linked, with beta-amyloid promoting the formation of tau tangles.
The new vaccine contains DNA coding for a segment of the beta-amyloid protein building block, or peptide.
In the study the vaccine triggered an immune response that not only led to a 40% reduction in beta-amyloid build-up, but also reduced tau formation by 50%.
The research was conducted on mice which were genetically engineered to develop a rodent equivalent of Alzheimer’s disease.
Lead scientist Dr Roger Rosenberg, director of the Alzheimer’s Disease Centre at the University of Texas in the US, said: “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.
“I believe we’re getting close to testing this therapy in people.”
A major obstacle to developing effective Alzheimer’s vaccines has been finding safe ways to introduce them to the body.
One previous experimental vaccine developed in the early 2000s caused brain swelling in some patients when tested on humans.
The new vaccine is injected into skin instead of muscle, which leads to a different kind of immune response.
If repeated in humans, the effects seen in mice would have “major therapeutic value”, said the researchers.
Co-author Dr Doris Lambracht-Washington, another member of the University of Texas team, said: “If the onset of the disease could be delayed by even five years, that would be enormous for the patients and their families.
“The number of dementia cases could drop by half.”
A number of drugs that target amyloid brain deposits and tau tangles are under development or in clinical trials.
But an effective vaccine would be a better strategy, according to the Texas scientists. It would be both more accessible and less expensive.
Earlier this year, the same team discovered the precise point at which a tau molecule becomes harmful but has not yet formed tangles in the brain.
The scientists are also working on a spinal fluid test that can detect abnormal tau before symptoms arise.
Such a test could identify people who have not yet displayed symptoms but have high levels of tau and amyloid in their brains. Patients singled out by the test could then be candidates for vaccine treatment.
Dr Rosenberg said: “The longer you wait, the less effect it will probably have. Once those plaques and tangles have formed, it may be too late.”
