NUNZIUM

Alzheimer's is a neurodegenerative disorder characterized by a progressive loss of memory and cognitive function, along with changes in behaviour and personality. It is the most common form of dementia, affecting millions of people worldwide, and is typically diagnosed in individuals over 65. However, early-onset forms of the disease can occur in younger individuals. Alzheimer's is caused by the accumulation of abnormal protein deposits in the brain, which can interfere with communication between brain cells and ultimately lead to their death. While the major hallmarks of Alzheimer's are well-known, we still have little idea what triggers it. Specific genes and lifestyle factors such as loneliness, lack of exercise and poor diet can all increase the risk of Alzheimer's, but how and why it begins remains a mystery.

Since the mid-80s, a handful of scientists worldwide have doggedly pursued the idea that either a virus or a bacterium could play a role in Alzheimer's. Studies show that people with herpes are more likely to get Alzheimer's. In particular, evidence pointed towards herpes simplex virus 1 (HSV-1) – a pathogen found in 70% of the UK population and the cause of oral herpes. When Prof Ruth Itzhaki from Oxford University's Institute of Population Ageing – who has done more than any other scientist to advance the HSV-1 theory of Alzheimer's - examined post-mortem brain samples from patients, she found more significant amounts of the virus's DNA than in people who had not died of the disease. Moreover, other studies show that treatment with a standard antiviral drug decreased the risk of dementia ninefold. Others have suggested that bacteria may also be capable of initiating the neurodegeneration that leads to Alzheimer's. Chlamydia pneumonia, which causes lung disease, and Borrelia burgdorferi, associated with Lyme disease and gum infections, have all been put forward as possible triggers. The main reason viruses like HSV-1 and possibly bacteria may be capable of triggering Alzheimer's is that they invade the body before burrowing into the central nervous system and travelling to the brain sometime in midlife. Once there, they stay dormant for many years before being reactivated in old age, either because the ageing immune system can no longer keep them in check or something else – a traumatic episode, a head injury or perhaps another infection – spurs them to life. Once awakened – so the theory goes – they begin to wreak havoc. Davangere Devanand, a neurologist at Columbia University Medical Center, is running a clinical trial investigating whether a herpes antiviral drug called valacyclovir could slow the progression of Alzheimer's in patients in the early stages of the disease. The ongoing trial, expected to be completed by early 2024, could significantly affect how we view the condition.