Links between pathogens and Alzheimer’s spur new projects searching for causal evidence
This week, thousands of researchers are flocking to downtown Philadelphia for what’s billed as the largest international conference dedicated to Alzheimer’s disease. But several kilometers away a much smaller group congregated for an alternative meetup: a daylong dive into whether and how pathogens might cause the fatal dementia.
Saturday’s gathering of about 80 scientists on the city’s periphery is something of a metaphor for where the idea sits in the larger Alzheimer’s community, long dominated by the view that the plaque-forming brain protein amyloid beta drives the disease. But the links between pathogens and Alzheimer’s appear to be slowly tightening. The COVID-19 pandemic lent momentum to the field: debilitating neurological symptoms, such as those in some people with Long Covid, reinforced that a virus can chronically disrupt the brain.
More recently scientists have found evidence that infection can mobilize a signature protein of Alzheimer’s called tau. And just last week they reported that a vaccine against shingles, caused by a virus that lurks in the nervous system, is associated with a lower dementia risk.
Just holding this meeting “has been such a turnaround,” said William Eimer, a Harvard University neuroscientist who presented the findings on tau there. He lamented “fighting uphill to get things published and get funded.” A 2-year-old effort called the Alzheimer’s Pathobiome Initiative (AlzPI), which spearheaded the meeting, now hopes to strengthen the case that pathogens play a role by encouraging specialists to swap samples and share data.
Eimer and his then-mentor Robert Moir found one clue in 2016, reporting that amyloid beta protected against infection in mouse and worm models of Alzheimer’s disease. The finding suggested pathogens might help mobilize the protein. And in 2018, they reported more direct evidence, showing that amyloid beta aggregates in the presence of herpes simplex virus-1 (HSV-1), another clue that the protein represents some kind of protective response.
In 2019, another team reported that Porphyromonas gingivalis, a bacterium that causes gum disease, appears in the brains of Alzheimer’s patients. When repeatedly applied to the gums of mice, it appeared to trigger Alzheimer’s pathology in their brains, including excess amyloid beta. A year later came news that HSV-1 could cause Alzheimer’s-like changes in a 3D stem-cell derived tissue culture meant to model human brain tissue. Numerous pathogens have been found to be more common in the brains of people who had Alzheimer’s than those who did not, including the bacterium Chlamydia pneumoniae, which causes respiratory infections. [Continue reading…]
Almost half of dementia cases worldwide could be prevented or delayed, a study has found, as experts named 14 risk factors.
The number of people living with dementia globally is forecast to nearly triple to 153 million by 2050, and researchers warn this presents a rapidly growing threat to health and social care systems. Global health and social costs linked to dementia exceed $1tn (£780bn) a year, the research shows.
However, in a seismic report published by the Lancet, 27 of the world’s leading dementia experts concluded that far more cases could be avoided or delayed than previously thought.
Addressing 14 modifiable risk factors, starting in childhood and continuing throughout life, could prevent or delay 45% of dementia cases, even as people live longer, the Lancet commission on dementia said. The findings were presented at the Alzheimer’s Association international conference in the US. [Continue reading…]