Chlamydia pneumoniae—a common bacterium that causes pneumonia and sinus infections—can linger in the eye and brain for years and may aggravate Alzheimer’s disease, according to a study from Cedars-Sinai. Published in Nature Communications, the discovery suggests this bacterium can amplify Alzheimer’s disease and points to potential interventions including inflammation-limiting therapies and early antibiotic treatment.
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Some people don’t develop dementia despite showing signs of Alzheimer’s disease in their brain, and we’re starting to understand why
Some people develop Alzheimer’s-related brain changes without experiencing symptoms of the disease, such as memory loss. We don’t know exactly why this occurs, but two recent studies are inching us closer towards an answer, with scientists revealing that these people have unusual changes in their brain that may shield them from cognitive decline.
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Cancer and Alzheimer’s disease are two of the most feared diagnoses in medicine, but they rarely strike the same person.
For years, epidemiologists have noticed that people with cancer seem less likely to develop Alzheimer’s, and those with Alzheimer’s are less likely to get cancer, but nobody could explain why.
A new study in mice suggests a surprising possibility: certain cancers may actually send a protective signal to the brain that helps clear away the toxic protein clumps linked to Alzheimer’s disease.
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Researchers have created a targeted compound that blocks an enzyme linked to inflammation in individuals with a genetic predisposition to Alzheimer’s disease, while still maintaining normal brain activity and successfully passing through the blood-brain barrier.
Scientists at the University of Southern California report that they have found new druglike compounds that could calm a major source of brain inflammation tied to Alzheimer’s disease. The study was just published in the Nature journal npj Drug Discovery.
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Alzheimer’s may destroy memory by flipping a single molecular switch that tells neurons to prune their own connections. Researchers found that both amyloid beta and inflammation converge on the same receptor, triggering synapse loss. Surprisingly, neurons aren’t passive victims—they actively respond to these signals. Targeting this receptor could offer a new way to protect memory beyond current amyloid-focused drugs.
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Some loved ones may struggle to recall what they ate for lunch just an hour ago, yet they can vividly describe a childhood vacation from fifty years ago. For many families navigating an Alzheimer’s diagnosis, this is one of the most perplexing symptoms — the loss of short-term memory vs. long-term recollection.
However, this selective memory loss is not random. According to G. Peter Gliebus, M.D., chief of neurology and director of Cognitive and Behavioral Neurology at Marcus Neuroscience Institute, part of Baptist Health, at Boca Raton Regional Hospital, there is a specific biological reason why the brain’s timeline seems to unravel from the present backward.
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