Introduction
The new millennia had just begun, the year was 2002, and there was huge excitement surrounding a potential vaccine designed to target Alzheimer’s disease. The AN1792 drug had reached its phase II clinical trial, however it was halted due to reports of swelling in the brain which was thought to worsen the disease.1
This drug held great potential and hope for an estimated 50 million dementia sufferers worldwide. A further 10 million new cases are reported every year2 and by 2050, the prevalence of Alzheimer’s disease is expected to quadruple.3
The Impacts of Alzheimer’s Disease
Alzheimer’s disease is the result of the formation of tangles (twisted protein strands) and plaques (abnormal protein clusters) in and around the brain’s nerve cells. These structures prevent cellular communication so the cells begin to lose their functionality and die, this is otherwise known as a form of neurodegeneration.4
Alzheimer’s and other dementia related diseases vary from person to person and patients can often suffer from mental health issues such as anxiety and depression.5,6,7 The progressive brain disorder can destroy mental capabilities, resulting in an inability to carry out daily activities, language problems and memory loss.6 A cognitive decline, such as that experienced by Alzheimer’s sufferers, can also lead to abnormal behaviours and personality changes, leading to greater frustration and additional stresses on daily life for patients and also their families.6,7
The AN1792 Trial
It was therefore understandable when many patients and their families looked to the AN1792 trial for hope, and its termination left many disappointed. Original reports suggested that the trial drug actually worsened the disease by overstimulating the immune response and causing inflammation in the brain.1,8 However, since then, there have been numerous follow up studies which counter this and actually suggest that the drug showed signs of working after all.8,9,10
Post-mortem pathological studies of patients involved in the original Phase 1 or 2 trials showed that the drug had noticeably reduced the levels of amyloid plaques from the brain.1,8,9,10 Amyloid plaques build up in the brains of Alzheimer’s patients and lead to the neurodegeneration we see so often in dementia sufferers. In fact, in a study by Nicoll et al. in 2019, researchers found that not only were these plaques reduced, but they had also continued to be kept low for 14 years since the trial ceased, this is thought to be due to the active nature of the vaccine.10 While this is exciting, it’s worth noting that cognitive decline was not cured and patients still suffered from dementia leading up to their death.
Where Are We Now?
These findings along with many other promising results have paved the way to where we are today. More drugs are reaching clinical trials, some of which are focusing on clearing the amyloid plaques inspired from the earlier AN1792 trials.11,12
While recent developments in the field provide fresh sources of hope for dementia sufferers and their loved ones, it’s important to consider that such research is dependent on those people who play a vital role in the trials. Having already suffered disappointment when the plug was pulled on AN1792, these groups continued to help in follow up studies, despite the natural uncertainties of new treatments and knowing it would not directly benefit them. By playing a vital role in Alzheimer’s research these people have helped to obtain results that we all hope will one day make a revolutionary change in the lives of Alzheimer’s sufferers and the future of humanity as a whole.
By Dan Lynes
