According to reports in New Scientist researchers are getting close to a major medical breakthrough in our ability to treat Alzheimer’s disease and other age-related neurodegenerative diseases.
The process of ageing or ‘senescence’ in the brain is different to most other parts of the body. In Alzheimer’s patients the brain cells, as a result of accumulated DNA damage, stop dividing and operating normally and instead start producing toxic proteins. As we grow older, our cells have divided more often and with each division there is a greater chance of there being some DNA damage. This damage can lead to a cell not developing normally and becoming a tumour. In response to this the body’s immune system is constantly monitoring for the presence of these cells in an attempt to deal with them before they grow into tumours.
Different mechanisms for dealing with old rogue cells have been identified. Apoptosis or cell suicide, allows affected cells to die off and then get ingested by the immune system. However, another mechanism is known as senescence, and this is where biological changes switch the cells into producing toxic proteins instead. This causes the destruction of nearby cells.
So, if senescence is a natural anti-cancer mechanism that has evolved to help people with a lower life expectancy, it just becomes more disadvantageous as we grow older. It is against this background that researchers are now looking into how these senescent brain cells could perhaps be the cause of destructive inflammation in Alzheimer's disease.
However, the mental function related cells in the brain, the neurons tend not to replicate and are therefore not as prone to the division-related ageing process. On the other hand, the neurons are surrounded by support cells called astrocytes, which make up around 80 – 90% of the brain.
In the most recent studies it has been found that healthy brains from people over 35 had up to 8 times more senescent cells than very young brains. They also found that in healthy brains of 80 and 90 year-olds, up to 30% of astrocytes had gone down the senescence route. But in people with Alzheimer's, this figure was about 10% higher.
The researchers therefore propose that an accumulation of senescent astrocytes "may link increased age and increased risk for sporadic Alzheimer's disease". According to New Scientist, the study provides a new way to look at Alzheimer's, and it might also shed light on other neurodegenerative diseases for which age is a risk factor.