Diabetes Raises Levels of Proteins Linked to Alzheimer’s Features

Growing evidence suggests that there may be a link between diabetes and Alzheimer’s disease, but the physiological mechanisms by which diabetes impacts brain function and cognition are not fully understood. In a new study published in Aging Cell, researchers at the Salk Institute for Biological Studies show, for the first time, that diabetes enhances the development of aging features that may underlie early pathological events in Alzheimer’s.

Specifically, the Salk team found increases in two hallmarks of Alzheimer’s-accumulations of amyloid beta (Abeta) and tau protein-in the brains of diabetic mice, especially in cells surrounding blood vessels. Abeta, the misfolded peptide that is thought in part to cause Alzheimer’s disease, aggregated inside astrocytes, star-shaped brain cells that, upon interaction with Abeta, release inflammatory molecules that can destroy neurons. Previously, this had not been shown in mouse models of type 1 diabetes (T1D).

"Our study supports and extends the links between diabetes, aging and Alzheimer’s," says senior author Pamela Maher, a senior staff scientist in Salk’s Laboratory of Cellular Neurobiology. "We show that type 1 diabetes increases vascular-associated amyloid beta buildup in the brain and causes accelerated brain aging."

The findings suggest that the neurovascular system may be a good candidate for new therapeutic targets to treat Alzheimer’s in the early stages of the disease.

How attention helps you remember: New study finds long-overlooked cells help the brain respond to visual stimuli

A new study from MIT neuroscientists sheds light on a neural circuit that makes us likelier to remember what we’re seeing when our brains are in a more attentive state.

The team of neuroscientists found that this circuit depends on a type of brain cell long thought to play a supporting role, at most, in neural processing. When the brain is attentive, those cells, called astrocytes, relay messages alerting neurons of the visual cortex that they should respond strongly to whatever visual information they are receiving.

The findings, published this week in the online edition of the Proceedings of the National Academy of Sciences, are the latest in a growing body of evidence suggesting that astrocytes are critically important for processing sensory information, says Mriganka Sur, the Paul E. and Lilah Newton Professor of Neuroscience at MIT and senior author of the paper.

Epileptic Fits Are Like Raging Thunderstorms: Astrocytes Help Reduce Long-Term Damage, Surprising New Research Shows

In the journal Experimental Neurology, the scientists report the beneficial effects of so-called astrocytes, a certain type of glial cells. They get their name from the Greek word for glue, as it was long thought that these cells simply hold the nerve cells together and provided them with nutrients. In the case of epilepsy, the prevalent opinion was that their reaction to a seizure would actually damage the brain. The researchers from Freiburg disagree. In fact, they say, astrocytes help to reduce long-term damage brought upon by epileptic fits.

The team discovered the positive effects of astrocytes in mice, in which epileptic states can be selectively triggered. If the scientists injected mice with a specific protein to activate the astrocytes prior to an epilepsy-inducing insult, fewer nerve cells died in the wake of the seizure. Other pathological changes that would usually occur in the brain were likewise significantly reduced. The astrocytes’ protective effect lasted for many days after their activation. When the researchers measured the rodents’ brain activity, they likewise found fewer signs that are typical for a brain suffering from epilepsy. However, the authors report that the astrocytes had to be already activated before seizures were elicited. Activating them afterwards, on the other hand, did not lead to a protective effect.

Further studies will have to demonstrate that astrocytes have this protective influence all over the brain. According to Haas, who is also a member of Freiburg’s new cluster of excellence BrainLinks-BrainTools, their findings suggest that a timely activation of astrocytes could offer an effective protection from long-term damage to the brain.

Cajal’s histological preparations and drawings showing some contributions to glial cells. (A) Fibrous astrocyte in the white matter of adult brain (formalin-uranium nitrate and gold-sublimated chloride); (B) Protoplasmic astrocyte in an adult brain (silver carbonate (del Rio) and formalin-uranium nitrate); (C) Twin astrocytes in the human hippocampus (formalin-uranium nitrate); (D) Fibrous astrocytes from the white substance of adult brain (Golgi methods); (E) Olygodendrocytes (ammoniacal silver oxide and Nissl); (F) Microglia cells (ammoniacal silver oxide, reduced silver nitrate and silver carbonate (del Rio) methods).

Source: The Histological Slides and Drawings of Cajal