About Alzheimer’s disease


Alzheimer’s disease is a progressive, fatal brain disease characterised by a decline in memory, language and other thinking skills, as well as changes in mood and behaviour. However, biological changes in the brain can occur even decades before the first symptoms appear. By the late stages of the disease, people are often unable to communicate and become completely reliant on others for even simple day-to-day tasks.1

A major global impact

Dementia affects 46.8 million people worldwide with an estimated cost of USD 818 billion. Alzheimer’s disease is the most common cause of dementia, with 9.9 million people newly diagnosed with dementia each year.1 There is no cure, which has become one of society’s greatest public health challenges. Current treatments focus on alleviating symptoms, but are unable to stop the disease from progressing because they do not affect the underlying causes.1 By 2050, more than 130 million people will have dementia.2

What causes this disease?

The underlying biology of Alzheimer’s disease is based on the build-up of two proteins – beta amyloid and tau – in the brain, usually caused by advanced age or genetic factors. One of the pathological hallmarks of Alzheimer’s disease is the accumulation of beta amyloid (increased production or reduced clearance) in the brain.1 While beta amyloid plaques are a hallmark of Alzheimer’s disease, beta amyloid exists in multiple forms, including monomers (single proteins), oligomers (small aggregates of proteins), fibrils (long aggregates of proteins), and plaques. It is unclear whether all or only some of these beta amyloid forms are damaging to the brain, but there is substantial evidence that aggregated forms, such as oligomers and plaques, are toxic to nerve cells.3

Our research and development

Our goal is to change how the disease affects the brain – not just treat symptoms. Roche’s research in Alzheimer’s disease encompasses several pathways implicated in the underlying biology of the disease, including beta amyloid and tau. Data generated by Roche, industry peers and the academic community suggest that removing different forms of beta amyloid may provide clinical benefit for people in the earlier stages of Alzheimer’s disease. Roche is evaluating new investigational medicines which target beta amyloid in different ways as well as pursuing research in other pathways implicated in Alzheimer’s disease, such as the build-up of tau.

In addition, Roche has a strong commitment to accurate and timely diagnosis, working with collaborators to innovate diagnostic technologies that can potentially help today’s patients receive better care and tomorrow’s patients receive effective treatments. New diagnostic tools coupled with novel targeted therapies will enable us to detect, measure, and slow the progression of this disease.  


1 Alzheimer’s Association. 2015 Alzheimer’s Disease Facts and Figures. Alzheimer’s & Dementia 2015; 11(3):332+.
2 Alzheimer’s Disease International. World Alzheimer Report 2015: The Global Impact of Dementia.  Last accessed on 1 July 2016.
3 Querfurth HW and LaFerla FM. Alzheimer’s Disease. N Engl J Med 2010; 362(4):329-44.