Researchers in the UK have used DNA sequencing to examine bacteria in post-mortem brains from patients with Alzheimer’s disease. Their findings suggest increased bacterial populations and different proportions of specific bacteria in Alzheimer’s, compared with healthy brains. The findings may support evidence that bacterial infection and inflammation in the brain could contribute to Alzheimer’s disease.
Alzheimer’s disease is a neurodegenerative disease that results in cognitive decline, and eventually death. In the brain, the disease causes neurons to die and break down, and involves high levels of a peptide called amyloid and aggregations of a protein called tau. However, scientists are coming to appreciate that inflammation may also play a role.
“Alzheimer’s brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate,” says David Emery, a researcher from the University of Bristol, and an author on the study, which was recently published in Frontiers in Aging Neuroscience.
So, what’s causing this inflammation? Some genetic risk-factors for Alzheimer’s disease can have effects on the inflammatory response, but infection may also play a role. “Neuroinflammation in the brain may be a reaction to the presence of bacteria,” says Emery. The brain is normally sealed behind specialized blood vessels that make it very difficult for things like bacteria in the blood to enter. However, at least one of the genetic risk-factors for Alzheimer’s disease may cause these blood vessels to lose some of their integrity, which could allow bacteria to enter and colonize the brain.
The research team set out to discover if there were any differences in the types of bacteria present in brains from Alzheimer’s disease patients and healthy brains. “Previous studies looking at bacteria in the Alzheimer’s brain have primarily investigated specific bacterial species,” explains Shelley Allen, another researcher involved in the study. “We wanted to use an unbiased method to obtain the fullest overview possible of the entire bacterial population in the Alzheimer’s brain, and compare these results with those from a healthy aged brain.”
The researchers analyzed eight Alzheimer’s and six healthy brain samples from a brain bank, where people donate their brains after death for medical research. They used a technique called next generation sequencing (NGS) to detect specific bacterial genes. “NGS technology allows millions of these DNA molecules to be sequenced at the same time, providing an unbiased overview of a complex bacterial population,” explains Allen.
They found that the Alzheimer’s brains contained different proportions of specific bacteria compared with the healthy brains. “Comparing the bacterial populations showed at least a tenfold higher ratio overall of Actinobacteria (mostly P. acnes) to Proteobacteria in the Alzheimer’s brain compared with the healthy brain,” says Emery. (I NOTE THAT THIS IS THE SAME BACTERIA THAT RYAN CARTY WROTE ABOUT. IT CAUSED THE WHIPPLES DISEASE HE IS FIGHTING, AND IT CAN CAUSE OR CONTRIBUTE TO SEVERE DEMENTIA).
However, the researchers were surprised to find that there also appeared to be more bacteria in the Alzheimer’s brains. “Unexpectedly, Alzheimer’s brains gave on average an apparent 7-fold increase in bacterial sequences above that seen in the healthy brain,” says Allen. “The healthy brains yielded only low levels of bacterial sequences, consistent with either a background signal or normal levels present in the blood stream in brain tissue.”
The team caution that the NGS method does not directly indicate actual bacterial numbers, and further work will be required to confirm that bacteria play an active role in Alzheimer’s disease. “We need quantitative studies on the bacterial presence in the brain,” says Allen. “Larger numbers of brain samples are required, and future studies should also investigate if bacteria are involved in other neurodegenerative diseases involving neuroinflammation.”
I’m always trying to figure out why I got this disease at a relatively younger age. Now I ponder the role of bacteria crossing my leaky brain barrier. My neurologist says I reached a threshold.
The greatest researchers and neurologists still have only clues. They know that Alzheimer’s brains show disproportionate amounts of Amyloid. They measure the amount of Amyloid and Tau in cerebral fluid. But bacteria colonizing the brain? Oddly, the insidious symptoms of progression began in me around mid 2015 a few months after beginning an invasive dental procedure for a dental implant. After a long period of great happiness and delightful high functioning, I suddenly could not handle my work load and the many demanding facets of my career.
With me the deterioration was sudden and has been quite rapid. It wasn’t only a matter of losing things and forgetting my keys. I did not find myself putting my shoes in the freezer. It was a full fledged breakdown in the ability to process my thoughts. My thinking became fragmented. At this point, I’ve lost many of my Instrumental Abilities of Daily Life (ex. I recently relearned how to make an omelet, and I was a gourmet cook. I have to put my clothing on a hanger for the next day, because when I get up I can’t figure out where anything is and dressing myself is a nightmare if I am not prepared. Glad I still can dress myself though!). That’s a rapid precipitous decline from my previous level of functioning, in which I was a world traveler and lecturer, professor, teacher and chair of my department.
Two and one half years is half the time in which the late great Pat Summit lived between diagnosis of EOAD and her death. It’s very scary and I admit I am scared as I witness the daily changes in my functioning, my physical body, my emotions and mood, my procedural, episodic, declarative and working memory. I’m a wife and mom, and a grandma of a 2 year old bundle of joy. True, I’ve had a “good run” as they say, I got to be past 60! My dear friend Moshe says, we are all here in the living room together, but there comes a time when we will have to say good night. But early onset AD is truly a horrible disease with no real treatment and as you all know, no cure. It destroys the life of a family as roles reverse, and children become parents, and spouses become caregivers. It decimates the family’s finances as I can attest to the stack of bills my poor husband is struggling to pay.
Something is causing the rapidly increasing numbers in people getting this disease, and it’s not just old age.
Bacteria in the brain causing the amyloid to grow and kill neurons, and as a result causing a cascade of neuro inflammation?