Alzheimer's Was Rare Thousands of Years Ago

Older people in ancient Greece and Rome may not have experienced severe memory problems like many who are aging today.

Researchers in California have combed through a slew of classical texts on human health written between the 8th century BCE and 3rd century CE, and found surprisingly few references to cognitive impairment in older folk.

According to Caleb Finch, who studies the mechanisms of aging at the University of Southern California, and historian Stanley Burstein from California State University, severe memory loss may have been an extremely rare outcome of growing old more than 2,000 years ago.   READ MORE...

A Drug for Alzheimer's

Rapamycin is also known as sirolimus and is sold under the brand name Rapamune.

An innovative strategy to lessen the plaques was also found in the study.

The oral administration of rapamycin to an Alzheimer’s disease mouse model induces an increase in beta (β)-amyloid protein plaques, according to researchers from The University of Texas Health Science Center at San Antonio (UT Health San Antonio). β-amyloid buildup is a hallmark of Alzheimer’s disease.



Rapamycin is FDA-approved for the treatment of transplant and cancer patients. The drug is also referred to as sirolimus and is sold under the name Rapamune. Publicly available data suggest that the drug might also improve learning and memory in aged mice. According to publicly accessible evidence, the medication may also boost learning and memory in elderly mice. The UT Health San Antonio researchers, on the other hand, discovered that following rapamycin administration, a protein called Trem2 (triggering receptor expressed on myeloid cells 2) is drastically reduced. Trem2 is found in microglia, immune cells found in the brain and spinal cord.

“Trem2 is a receptor located on the surface of the microglia, and it enables these cells to engulf and degrade β-amyloid,” said study senior author Manzoor Bhat, Ph.D. “Loss of Trem2 in microglia impairs the vital function of amyloid degradation, which in turn causes a buildup of β-amyloid plaques.” Dr. Bhat is professor and chairman of the Department of Cellular and Integrative Physiology at UT Health San Antonio and vice dean for research in the university’s Joe R. and Teresa Lozano Long School of Medicine.

Drug target
Importantly, the study, recently published in the Journal of Neuroscience, also featured a novel way to increase Trem2 in microglia. When the study lead author, Qian Shi, PhD, assistant professor in the Department of Cellular and Integrative Physiology, deleted a gene called Tsc1 from the microglia, there was a marked increase in Trem2 levels and a decrease in β-amyloid plaques.

Previous research has shown that loss of Tsc1 leads to activation of the mTOR (mammalian target of rapamycin) signaling pathway. Rapamycin, in contrast, blocks this pathway. “We expected that selective loss of Tsc1, only in microglia and not in neurons or other cells, would have negative consequences because inhibiting mTOR with rapamycin has known therapeutic uses in some disease models,” Dr. Shi said. “But the opposite was occurring.” Thus, repressing Tsc1 solely in microglia to enhance β-amyloid uptake could be a potential drug target, Dr. Shi said.  READ MORE...

Common Viruses and Alzheimer's

Varicella zoster virus (VZV), which commonly causes chickenpox and shingles, activates herpes simplex virus (HSV) from dormancy in neural tissue grown in vitro, which then leads to an increase in plaque deposits and decrease in neural signaling — hallmarks of Alzheimer’s disease. Credit: Tufts University

Shingles infection may awaken dormant neurological herpes viruses, causing inflammation and accumulation of Alzheimer’s associated proteins in the brain.

Alzheimer’s disease is the most common cause of dementia in older adults and the 7th leading cause of death in the United States, according to the National Institute on Aging. 

It is a debilitating progressive illness that slowly destroys cognitive function and memory.

It can begin almost imperceptibly, often masquerading in the early months or years as forgetfulness that is very common in older age. What causes Alzheimer’s disease remains largely a mystery.

But researchers using a three-dimensional human tissue culture model mimicking the brain, have shown that varicella zoster virus (VZV), which commonly causes chickenpox and shingles, may activate herpes simplex (HSV), another common virus, to set in motion the early stages of Alzheimer’s disease. 

The study was conducted by scientists at Tufts University and the University of Oxford.  READ MORE...

Diagnosing Alzheimer's Quickly

A new machine learning algorithm can diagnose Alzheimer’s disease from a single MRI brain scan, 

using a standard MRI machine available in most hospitals.

New research breakthrough uses machine learning technology to look at structural features within the brain, including in regions not previously associated with Alzheimer’s. The advantage of the technique is its simplicity and the fact that it can identify the disease at an early stage when it can be very difficult to diagnose.

Although there is no cure for Alzheimer’s disease, getting a diagnosis quickly at an early stage helps patients. It allows them to access help and support, get treatment to manage their symptoms and plan for the future. Being able to accurately identify patients at an early stage of the disease will also help researchers to understand the brain changes that trigger the disease, and support development and trials of new treatments.

The research was published today (June 20, 2022) in the Nature Portfolio Journal, Communications Medicine, and funded through the National Institute for Health and Care Research (NIHR) Imperial Biomedical Research Center.


Alzheimer’s disease is the most common form of dementia, affecting over half a million people in the UK. Although most people with Alzheimer’s disease develop it after the age of 65, people under this age can develop it too. The most frequent symptoms of dementia are memory loss and difficulties with thinking, problem solving and language.  READ MORE...

Cause of Alzheimer's

Scientists in California tried to study Alzheimer’s disease from a different perspective and the results may have led them to the cause of the disease.

Researchers at the University of California- Riverside (UCR) recently published results from a study that looked at a protein called tau. By studying the different forms tau proteins take, researchers discovered the difference between people who developed dementia and those who didn’t.

The tau protein was critical for researchers because they wanted to understand what the protein could reveal about the mechanism behind plaques and tangles, two critical indicators doctors look for when diagnosing people with Alzheimer’s.

By analyzing donated brain samples, researchers found that those with brain buildup, like plaques and tangles, but had no dementia had a normal form of tau. However, those who had a “different-handed” form of tau and developed plaques or tangles did have dementia.

Ryan Julian, a chemistry professor at UCR, said in a press release, “roughly 20% of people have the plaques, but no signs of dementia. This makes it seem as though the plaques themselves are not the cause.”

The amino acids that make up proteins like tau can either be right-handed or left-handed isomers, and normally proteins in living things are made from all left-handed amino acids, explained Julian.

However, most proteins only survive for less than 48 hours in the body, and if they hang around too long, certain amino acids can convert into the other-handed isomer. So that means a left-handed isomer could inadvertently convert into a right-handed isomer, which can lead to serious problems.

“If you try to put a right-handed glove on your left hand, it doesn’t work too well. It’s a similar problem in biology; molecules don’t work the way they’re supposed to after a while because a left-handed glove can actually convert into a right-handed glove that doesn’t fit,” said Julian.  READ MORE...

Breakfast Habits

Inflammation can be a tricky issue. On the one hand, it is a necessary process that our bodies need to heal from injury, which is known as acute inflammation. On the other, it can lead to serious health issues and illness if it turns chronic, which is the type we will be referring to in this article.

Chronic inflammation can be caused by things like autoimmune disorders, exposure to toxins, obesity, and an inactive lifestyle, and according to Harvard Health, it "plays a central role" in diseases like diabetes, heart disease, certain cancers, and Alzheimer's.

Because of inflammation's connection to weight, diet, and exercise, there are certain foods that we can eat and avoid to help lower our chances of developing chronic inflammation in the long run.

Continue reading to learn about some of the worst breakfast foods and breakfast habits for inflammation, and for more tips on inflammation, make sure to check out Popular Foods For Reducing Inflammation After 50.

Eating refined carbohydratesShutterstock

When it comes to inflammation, added sugar and refined carbohydrates are some of the leading culprits.

"One of the worst breakfast habits for inflammation is eating refined carbohydrates and foods high in added sugar like packaged pastries, donuts, and baked goods," says Amy Goodson, MS, RD, CSSD, LD author of The Sports Nutrition Playbook.

Lauren Manaker, MS, RDN, registered dietitian on our medical expert board and author of The First Time Mom's Pregnancy Cookbook and Fueling Male Fertility agrees, saying that "sugary and refined pastries like donuts and muffins can be loaded with ingredients that can contribute to inflammation, so it's best to stick to whole grain options without questionable ingredients instead."  READ MORE...