Lifeboat Foundation

Mild, persistent inflammation in tissue is considered one of the biological hallmarks of the aging process in humans—and at the same time is a risk factor for diseases such as Alzheimer’s or cancer. Prof. Francesco Neri and Dr. Mahdi Rasa of the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena have succeeded for the first time in describing at the molecular level the regulatory network that drives the general, multiple-organ inflammatory response. Moreover, they were able to show that dietary restriction can influence this regulatory circuit, thereby inhibiting inflammation.

Inflammation is an immune response of the body that is, in itself, useful: our immune system uses it to fight pathogens or to remove damaged cells from tissue. Once the immune cells have done their work, the inflammation subsides: the infection is over, the wound is healed. Unlike such acute inflammations, age-related chronic inflammation is not local. The innate immune system ramps up its activity overall, resulting in chronic low-grade inflammation. This aging-related inflammation is also known as inflammaging.

Summary: In mice genetically more susceptible to PTSD following a stressful event, researchers found an increased expression of cortisol receptors on neurons in the CA1 region of the dorsal hippocampus. Those increased receptors enabled an elevated expression of the HCN1 protein and TRIP8b, reducing neural excitability.

Source: medical college of georgia at augusta university.

Social avoidance is a common symptom of PTSD, and scientists working to better understand why have laboratory evidence that while stress hormone levels consistently increase in the immediate aftermath of a traumatic event, there can be polar opposite consequences in parts of the brain down the line.

Most of us consider nightmares pretty harmless, but apparently, they can be a bad sign. According to research at the University of Birmingham, people who experience frequent bad dreams in middle age are more likely to be diagnosed with dementia later in life.

New research suggests nightmares may become common several years or even decades before the characteristic memory and thinking problems of dementia set in. The study will be published today (September 21, 2022) in The Lancet.

Founded in 1,823 by Thomas Wakley, The Lancet is a weekly peer-reviewed general medical journal. It is one of the world’s oldest, most prestigious, and best known general medical journals. The journal publishes original research articles, review articles (“seminars” and “reviews”), editorials, book reviews, correspondence, as well as news features and case reports. The Lancet has editorial offices in London, New York, and Beijing.

Emmanuel Mignot and Masashi Yanagisawa won the 2023 Breakthrough Prize in life sciences for their discovery of the molecular mechanisms in the brain that cause the sleep disorder narcolepsy.

Summary: New research in cloned pigs with a mutation of the SORL1 sheds light on Alzheimer’s development. The findings could pave the way for new treatments for the neurodegenerative disorder.

Source: Aarhus University.

For decades, researchers from all over the world have been working hard to understand Alzheimer’s disease. Now, a collaboration between the Department of Biomedicine and the Department of Clinical Medicine at Aarhus University has resulted in a flock of minipigs that could lead to a major step forward in the research and treatment of Alzheimer’s.

Summary: The Allen Institute is launching a new global collaboration to map approximately 200 billion cells in the human brain by type and function.

Source: Allen Institute.

Scientists at the Allen Institute are launching the brain equivalent of the Human Genome Project, leading a new global collaboration to map the approximately 200 billion cells in the human brain by their type and function.

Summary: Researchers successfully turned skin cells from Parkinson’s patients into dopaminergic neurons by introducing a combination of neural-inducing genes into the skin cells.

Source: international society for stem cell research.

The possibility to make virtually all cell types of the human body from induced pluripotent stem cells (iPSCs), which are embryonic-like cells generated from a patient’s skin, in a process called reprogramming, has opened new avenues for disease modeling in the lab.

Small but mighty, lysosomes play a surprisingly important role in cells despite their diminutive size. Making up only 1–3% of the cell by volume, these small sacs are the cell’s recycling centers, home to enzymes that break down unneeded molecules into small pieces that can then be reassembled to form new ones. Lysosomal dysfunction can lead to a variety of neurodegenerative or other diseases, but without ways to better study the inner contents of lysosomes, the exact molecules involved in diseases—and therefore new drugs to target them—remain elusive.

A new method, reported in Nature on Sept. 21, allows scientists to determine all the molecules present in the lysosomes of any cell in mice. Studying the contents of these molecular recycling centers could help researchers learn how the improper degradation of cellular materials leads to certain diseases. Led by Stanford University’s Monther Abu-Remaileh, institute scholar at Sarafan ChEM-H, the study’s team also learned more about the cause for a currently untreatable neurodegenerative disease known as Batten disease, information that could lead to new therapies.

“Lysosomes are fascinating both fundamentally and clinically: they supply the rest of the cell with nutrients, but we don’t always know how and when they supply them, and they are the places where many diseases, especially those that affect the brain, start,” said Abu-Remaileh, who is an assistant professor of chemical engineering and of genetics.

For the memory prosthetic, the team focused on two specific regions: CA1 and CA3, which form a highly interconnected neural circuit. Decades of work in rodents, primates, and humans have pointed to this neural highway as the crux for encoding memories.

The team members, led by Drs. Dong Song from the University of Southern California and Robert Hampson at Wake Forest School of Medicine, are no strangers to memory prosthetics. With “memory bioengineer” Dr. Theodore Berger—who’s worked on hijacking the CA3-CA1 circuit for memory improvement for over three decades—the dream team had their first success in humans in 2015.

The central idea is simple: replicate the hippocampus’ signals with a digital replace ment. It’s no easy task. Unlike computer circuits, neural circuits are non-linear. This means that signals are often extremely noisy and overlap in time, which bolsters—or inhibits—neural signals. As Berger said at the time: “It’s a chaotic black box.”