Alzheimer's in the News - February 2025

The Alzheimer’s Hub of Hope has four sections: Heroes, Highlights, Headlines and Helpers/Caregivers. This post is aligned to the headlines section.

Mar 11, 2025

Here are the most interesting Alzheimer’s articles for February. I’ve summarized a few of them but you are encouraged to click on the underlined headings and read the items for yourself.

magazine pile lot — Photo by Waldemar on Unsplash

Study finds nearly 70% of suspected frontotemporal dementia patients were misdiagnosed

I started including frontotemporal dementia (FTD) in my posts several months ago based on a request from one of my subscribers. During my initial investigation, I learned that FTD is often misdiagnosed as Alzheimer’s. In my initial post on FTD (here) I stated:

“Many people, even medical practitioners, confuse FTD with AD since it is a type of dementia that typically occurs later in life (although often earlier than AD) and is relatively rare with only 50,000 sufferers in the United States compared to 6.7 million for AD per ChatGPT.
Because of frequent misdiagnosis, Deborah Kan, one of my Alzheimer’s Heroes of Hope, has updated her Being Patient site to include a ~10 minute FTD interactive learning guide.

The Association for Frontotemporal Degeneration (AFTD) has a wealth of information on the disease and how it is different than Alzheimer’s. They offer 2-page “cheat sheets” to be used by health care providers during the diagnosis process to help them differentiate between FTD and AD. Therefore I’m not surprised that Australian research identified a 70% misdiagnosed error rate.

The Cause of Alzheimer's Might Be Coming From Inside Your Mouth

In recent years, a growing number of scientific studies have backed an alarming hypothesis: Alzheimer's disease isn't just a disease, it's an infection.

While the exact mechanisms of this infection are something researchers are still trying to isolate, numerous studies suggest the deadly spread of Alzheimer's goes way beyond what we used to think.

One such study, published in 2019, suggested what could be one of the most definitive leads yet for a bacterial culprit behind Alzheimer's, and it comes from a somewhat unexpected quarter: gum disease.

In a paper led by senior author Jan Potempa, a microbiologist from the University of Louisville, researchers reported the discovery of Porphyromonas gingivalis – the pathogen behind chronic periodontitis (aka gum disease) – in the brains of deceased Alzheimer's patients.

It wasn't the first time the two factors have been linked, but the researchers went further.

In separate experiments with mice, oral infection with the pathogen led to brain colonization by the bacteria, together with increased production of amyloid beta (Aβ), the sticky proteins commonly associated with Alzheimer's.

"Infectious agents have been implicated in the development and progression of Alzheimer's disease before, but the evidence of causation hasn't been convincing," Dominy said at the time.

"Now, for the first time, we have solid evidence connecting the intracellular, Gram-negative pathogen, P. gingivalis, and Alzheimer's pathogenesis."

In addition, the team identified toxic enzymes called gingipains secreted by the bacteria in the brains of Alzheimer's patients, which correlated with two separate markers of the disease: the tau protein, and a protein tag called ubiquitin.

But even more compellingly, the team identified these toxic gingipains in the brains of deceased people who were never diagnosed with Alzheimer's.

I’ve posted about the link between dental health and AD here.

Air Pollution May Cause Alzheimer's Disease, But There May be a Solution

While the connection between air pollution and lung disease could appear obvious, the link between breathing in toxins and suffering memory loss looks about as clear as a cloud of cigarette smoke.

Scientists at Scripps Research Institute first identified how contaminants in smog, pesticides, and other airborne chemical can affect the brain. Now they have identified a way to potentially reverse those effects, they report in the Proceedings of the National Academy of Sciences.

A chemical process in the brain called S-nitrosylation — which can be activated by inflammations as well as a variety of airborne toxins — blocks brain cells from making new connections, leading to brain cell death, then memory loss. Blocking S-nitrosylation in a specific brain protein partially reverses memory loss in mouse models for Alzheimer’s disease.

“We’ve revealed the molecular details of how pollutants can contribute to memory loss and neurodegenerative disease,” Stuart Lipton, a Scripps neuroscientist and an author of the study, said in a press release. “This could ultimately lead to new drugs that block these effects to better treat Alzheimer’s disease.”

Studies have already established that environmental toxins lead to higher NO levels in the brain. The new work strengthens the hypothesis that these toxins can accelerate brain aging and Alzheimer’s through S-nitrosylation.

Therefore, preventing that process in critical brain proteins could slow or prevent brain damage in Alzheimer’s patients. The group is now developing drugs to block key S-nitrosylation reactions.

Drugs that reduce dementia risk — and others that increase it

Some medications could have the unintended benefit of reducing dementia risk. That’s according to a recent study by the universities of Cambridge and Exeter, where researchers evaluated several existing drugs to see if they could do double-duty as dementia treatments.

The team reviewed data from 14 prior studies, which included more than 130 million patients and one million dementia cases, according to a press release.

They determined that several classes of prescription drugs were shown to affect dementia risk.

"If we can find drugs that are already licensed for other conditions, then we can get them into trials and — crucially — may be able to make them available to patients much, much faster than we could do for an entirely new drug."

Drugs and vaccines that were linked to reduced risk of dementia are:

Drugs: Antibiotics, antivirals, anticoagulants (blood thinners) and anticonvulsants (medications used to prevent or treat seizures).
Vaccines: hepatitis A, typhoid, hepatitis A and typhoid combined, and diphtheria.

This finding supports the hypothesis that common dementias may be triggered by viral or bacterial infections.

Anti-inflammatory medications, such as ibuprofen, were also found to reduce dementia risk.

Some drugs were associated with an increased risk of dementia, including antipsychotic medications. There was "conflicting evidence" for other classes of drugs, including those indicated for blood pressure, depression and diabetes.

Herpes viruses may contribute to Alzheimer's disease via transposable elements

University of Pittsburgh researchers uncovered a surprising link between Alzheimer's disease and herpes simplex virus-1 (HSV-1), suggesting that viral infections may play a role in the disease.

The study also revealed how tau protein, often viewed as harmful in Alzheimer's, might initially protect the brain from the virus but contribute to brain damage later.

"Our study challenges the conventional view of tau as solely harmful, showing that it may initially act as part of the brain's immune defense," said senior author Or Shemesh, Ph.D., assistant professor in the Department of Ophthalmology at Pitt. "These findings emphasize the complex interplay between infections, immune responses and neurodegeneration, offering a fresh perspective and potential new targets for therapeutic development."

The scientists identified forms of HSV-1-related proteins in Alzheimer's brain samples, with greater amounts of viral proteins co-localized with tangles of phosphorylated tau—one of the hallmarks of Alzheimer's disease pathology—in brain regions especially vulnerable to Alzheimer's across disease stages.

Further studies on miniature models of human brains in a Petri dish suggested that HSV-1 infection could modulate levels of brain tau protein and regulate its function, a protective mechanism that seemed to decrease post-infection death of human neurons.

I posted about how infections, including herpes, could be the cause of AD here.