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Alzheimer’s Disease and Dementia can be caused by infections that are curable, propose scientists
Progressive brain disorder Alzheimer’s Disease that results in the loss of memory and cognitive skills – Dementia – could be caused by infectious diseases and, therefore, reversible.
A group of international scientists collaborating on this potentially world-changing research have formed the Alzheimer’s Pathobiome Initiative (AlzPI) to understand the role of microbes in the brain, devise ways to diagnose and treat brain infections, as well as identify preventative measures, including vaccines. There is research to show that shingles vaccines have been successful in lowering the risk of dementia, for example.
Currently there is no cure or effective therapy for Alzheimer’s Disease, which is a major cause of morbidity and mortality. Although there is an inherited and ageing element to the disease, there's an increasing body of research which points to microbial infections of the brain leading to dementia. Even when Alois Alzheimer first discovered the disease, in 1906, he suspected that microbes were involved, but he wasn’t able to follow it up since it’s difficult to access the brain microbiome.
The AlzPI says a causal role for infection in Alzheimer’s Disease is contentious and funding has been hard to come by. Many remain sceptical, and this is fuelled by the technical difficulties in diagnosing and treating brain infections.
The team have written a research paper Establishment of a consensus protocol to explore the brain pathobiome in patients with mild cognitive impairment and Alzheimer’s disease which says there are now multiple findings which support the hypothesis that the disease can be caused by infection.
Data has recently emerged that the signature protein of the Alzheimer’s Disease brain, Aß peptide, has an important physiological role in the immune system, by forming extracellular traps that deactivate pathogens and protect host cells from infection.
In Alzheimer’s Disease, failure of this immune response, or persistent activation from chronic infection, leads to sustained inflammation and neurodegeneration.
A research paper entitled The remarkable complexity of the brain microbiome in health and disease looked into microbes in the human brain and their contribution to neurodegenerative conditions, supporting the contention that infection – perhaps associated with declining immunity with age – may contribute to Alzheimer’s Disease development.
Researchers discovered that some microbes are over-represented in Alzheimer’s brains, including the bacteria Streptococcus and Staphylococcus, as well as fungi from the Candida and Cryptococcus groups that are all related to known human pathogens (an organism that causes disease). Also, an algae-related species that needs more research was more abundant in Alzheimer’s Disease brain samples.
A report in Science Advisor says that scientists have found evidence that infection can mobilise a signature protein of Alzheimer’s Disease, called tau. William Eimer, the Harvard University neuroscientist involved in this research says findings suggested pathogens might help to mobilise tau.
Research undertaken in 2019 showed that a bacterium which causes gum disease also appears to trigger the Alzheimer’s pathology and spark the onset of the disease.
Numerous pathogens have been found to be more common in the brains of people who suffer from Alzheimer’s Disease than those who don’t, including Chlamydia pneumoniae, which causes respiratory infections.
The AlzPI says there's an urgent need for interdisciplinary collaboration, to test and validate the best methods to characterise the brain pathobiome and identify the least invasive biosample to be collected from patients to unveil microbial infection.
It also calls for a multi-centre study to test post mortem biosamples to reveal microbes. The findings could be used prospectively in patients with mild cognitive impairment or early Alzheimer’s Disease to reveal potential microbial infections and tailor treatment to potentially reverse dementia.
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