It is more than 150 years since scientists proved that invisible germs could cause contagious illnesses such as cholera, typhoid, and tuberculosis. The role of microbes in these diseases was soon widely accepted, but "Germ Theory" has continued to surprise ever since – with huge implications for many apparently unrelated areas of medicine.
It was only in the 1980s, after all, that two Australian scientists found that Helicobacter Pylori triggers stomach ulcers. Before that, doctors had blamed the condition on stress, cigarettes and booze. Contemporary scientists considered the idea to be "preposterous", yet it eventually earned the Nobel Prize for Physiology or Medicine in 2005.
The discovery that the human papillomavirus can cause cervical cancer proved to be similarly controversial, but vaccines against the infection are now saving thousands of lives. Scientists today estimate that around 12% of all human cancers are caused by viruses.
We may be witnessing a similar revolution in our understanding of Alzheimer's disease. Lifestyle and genetic factors certainly play a role in the development of the illness. But it looks increasingly possible that some common viruses and bacteria – the kinds that give us cold sores and gum disease – may, over the long term, trigger the death of neural tissue and a steady cognitive decline. If so, infections may be one of the leading causes of the dementia.
Like the germ theories of ulcers and cancers, this hypothesis was once considered a kind of heresy – yet a string of compelling findings has sparked renewed interest in microbes' contributions to dementia. "There's a huge amount of work being done now, compared to even five years ago," says Ruth Itzhaki, an emeritus professor at the University of Manchester in the UK, who has spent three decades investigating the role of infection in Alzheimer's.
[---]
Scientists studying Alzheimer's have also struggled to explain why some people develop the disease while others don't. Genetic studies show that the presence of a gene variant – APOE4 – can vastly increase someone's chances of building the amyloid plaques and developing the disease. But the gene variant does not seal someone's fate as many people carry APOE4 but don't suffer from serious neurodegeneration. Some environmental factors must be necessary to set off the genetic time bomb, prompting the build-up of the toxic plaques and protein tangles.
[---]
Could certain microbes act as a trigger? That's the central premise of the infection hypothesis.
Itzhaki has led the way with her examinations into the role of the herpes simplex virus (HSV1), which is most famous for causing cold sores on the skin around the mouth. Importantly, the virus is known to lie dormant for years, until times of stress or ill health, when it can become reactivated – leading to a new outbreak of the characteristic blisters.
While it had long been known that the virus could infect the brain – leading to a dangerous swelling called encephalitis that required immediate treatment – this was thought to be a very rare event. In the early 1990s, however, Itzhaki's examinations of post-mortem tissue revealed that a surprising number of people showed signs of HSV1 in their neural tissue, without having suffered from encephalitis.
Importantly, the virus didn't seem to be a risk for the people without the APOE4 gene variant, most of whom did not develop dementia. Nor did the presence of APOE4 make much difference to the risk of people without the infection. Instead, it was the combination of the two that proved to be important. Overall, Itzhaki estimates that the two risk factors make it 12 times more likely that someone will develop Alzheimer's, compared to people without the gene variant or the latent infection in their brain.
- More Here
No comments:
Post a Comment