Infections Can Cause Brain Atrophy And Dementia
11/05/2024
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“We could certainly slow the aging process down if it had to work its way through Congress.”
-Will Rogers
Two provocative areas of research have led to the notion that infection could be a risk factor for dementia. On one hand, some studies have directly suggested that there is a possible link between some infections and an increased risk for Alzheimer’s disease (AD). Then, other studies found that two vaccines, the flu shot and the shingles vaccine, reduced the risk of dementia. Together, all this led to the hypothesis that infection might play a role in neurodegenerative diseases. This is now bolstered by a new study published last August in Nature Aging that identifies possible post-infection immunological/inflammation drivers that lead to brain atrophy and subsequent cognitive decline.
Brain atrophy! It can easily be detected via modern imaging technology, and it is not good.
We have abundant evidence that even minor infections can change the way we think and behave. More-severe infections that result in delirium have long been associated with long-term cognitive problems. Even shingles, which is a very painful relapse of chicken pox (you never clear the virus, which resides in your nerves) also is associated with dementia. There is a very effective vaccine that stops shingles in its tracks and it has been shown to reduce the risk for dementia later in life by up to 50%. The more severe an acute infection or its relapse, the greater the inflammation caused by the immune response, and the greater the risk of Alzheimer’s and other types of dementia. Therefore, it makes abundant sense that vaccines, which greatly reduce the severity of infectious disease, would also lessen the risk for dementia as well as for other long term post-infection health problems such as diabetes, Parkinson’s diesease, and maybe cancer that I have mentioned in these pages.
The link between infection and cognitive problems seems to hold with different types of infections, whether they are bacterial or viral. Of the 15 types of infections studied, six—flu, herpes (which includes small pox, chicken pox, shingles, etc.), respiratory tract infections, and skin infections—were associated with increased risk of atrophy in the brain’s temporal lobe. This region includes the inner folds of the temporal lobe where a rather small organ called the hippocampus sits on each side of the brain. This is part of what is called the limbic system, which manages the functions of feeling and reacting, and helps us process and retrieve two types of memory, declarative memories and spatial relationships.
Declarative memories are those related to facts and events such as learning how to memorize speeches or lines in a play. Spatial relationship memories involve pathways or routes. For example, when a cab driver learns a route through a city, they use spatial memory and that learning can actually increase the size of the hippocampus. Spatial relationship memories appear to be stored in the right hippocampus. In addition, short-term memories are converted into long-term memories in the hippocampus, but are then filed away long-term elsewhere in the brain. So, with a malfunctioning hippocampus, these short term memories do not get stored. And we forget things.
We have known about the hippocampus (or hippocampi, since we have two of them) for more than four centuries. The surgeon, Julius Caesar Arantius, first discovered the hippocampus in 1587, coining the term from the Greek word for seahorse (hippokampos) based on its shape. It does resemble a seahorse. This region, critical for memory and learning, is strongly affected in AD where the shrinking size of the hippocampus can be used to monitor the progress of the disease.
The latest study relating infection to dementia was based on data from the Baltimore Longitudinal Study of Aging, one of the longest-running studies of human aging in the United States. They also used neuroimaging to track how brain volume changed in 982 adults, with or without a history of infection. This began in 2009 and its data confirmed findings from analyses of UK Biobank data of almost 500,000 people, and a Finnish dataset of almost 300,000 subjects, both of which identified these infections as risk factors for dementia.
Of course, most of these studies were done before COVID. COVID has not been around long enough to definitely tell us whether the disease is also linked with increased risk of dementia, but as a respiratory infection accompanied by severe systemic inflammation, we can expect it to be.
Bottom line: Vaccines not only protect against the acute infection they were made for, but they also protect against serious post-infection complications such as new onset diabetes, Parkinson’s disease, perhaps cancer, and other long term complications of infectious disease, which now also includes dementia.
Get vaccinated!