A giant leap towards a cure for Alzheimer’s disease (and one step back)

Adopting a healthy lifestyle…

A CURE for dementia remains elusive, but a team led by Michael Heneka of the University of Bonn, Germany has a made massive step forward in understanding the mechanism in the brain that causes damage.

They have found a process by which inflammation triggers the build-up of amyloid-ß protein plaques in the brains of people with Alzheimer’s disease.

In people with Alzheimer’s disease, aggregates of amyloid-ß protein build up in the brain to form plaques, leading to nerve cell damage and memory loss.

Inflammation is thought to have a role, but the exact nature of its involvement has been hard to pin down.

Professor Heneka and colleagues have show in mice that inflammatory cues trigger immune cells called microglia to release specks of a protein called ASC.

This binds to the amyloid-ß protein and promotes the aggregation of amyloid-ß clusters in the brain.

When they applied an antibody to prevent ASC from binding to amyloid-ß, it reduced the formation of plaques in both cultured cells and in live mice.

The authors think that this process occurs in the very early stages of Alzheimer’s disease.

The paper was published in the prestigious international science weekly Nature, last month.

Professor Bryce Vissel, head of neuroscience and regenerative medicine in the Faculty of Science at the University of Technology, Sydney said this is an extremely important study for understanding Alzheimer’s disease.

“This comprehensive and elegant study from Michael Heneka’s group provides strong evidence in support of a disease mechanism and a new approach for treating Alzheimer’s disease,” he said.

“For decades, Alzheimer’s researchers have considered that amyloid is the cause of Alzheimer’s disease. This is in part because amaloid plaques are often seen in the brains of people with Alzheimer’s. It is not truly known what causes the plaques or whether amyloid causes Alzheimer’s disease.

“Despite this, there have been numerous failed attempts to develop drugs that remove amyloid from the brain of Alzheimer’s patients. Therefore we are looking for new approaches to both explain and block the disease.

“Our group has long been suggesting that inflammation is a key mediator of Alzheimer’s disease. This study showed the first direct link between inflammation and amyloid deposition.

“Interestingly, blocking speck formation prevented the spread of the amyloid in the brain and also reduced the extent of Alzheimer’s-like symptoms.

“This paper therefore clearly shows that ASC speck formation is instrumental in disease process showing unequivocally a link between inflammation and Alzheimer’s disease. This suggests a very exciting new way of thinking about the disease and treating it,” he said.

Meanwhile researchers from the Minnesota Evidence-based Practice Center (EPC) have reviewed published research of interventions aimed to help to prevent dementia in patients.

None of them worked.

Physical activity

Sixteen trials compared physical activity with an inactive control.

There was little evidence for the effectiveness of aerobic training, resistance training, or tai chi for improving cognition, although combining different types of interventions at the same time, such as physical activity, diet, and brain training, slightly improved cognitive test performance.

Prescription medications

Data from 51 trials comparing the effect of prescription medication with placebo or usual care on cognitive outcomes did not support the use of any known pharmacologic treatments in people with normal or mild cognitive impairment.

Brain training

Eleven trials of adults found insufficient evidence that cognitive training exercises could prevent dementia.

Group cognitive training improved performance only in the actual domain trained.

For example, memory training improved memory, but did not improve any other aspects of cognition.

Over-the-counter vitamins and supplements

Nearly 40 trials compared over-the-counter (OTC) supplements, including omega-3 fatty acids, soy, ginkgo biloba, B vitamins, vitamin D plus calcium, vitamin C or beta carotene or multi-ingredient supplements with placebos, for preventing or delaying cognitive decline. There was little evidence to suggest that any of these worked.

The researchers found that none of these interventions improved cognition.

But it could also be that the interventions started too late in life or for too short a time.

They said adopting a healthy lifestyle earlier in life may protects against dementia in later life.

Moreover it is unlikely to worsen cognition and may have other health benefits.

The findings were published in Annals of Internal Medicine last year.