Lifeboat Foundation

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.”

The pursuit of a cure for Alzheimer’s disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.

In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s, may have been based on fabricated data.

One year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer’s, even though the data supporting its use were incomplete and contradictory.

A new study recently published in Neurology, the medical journal of the American Academy of Neurology, suggests that physical and mental activities, such as doing chores around the home, exercising, and visiting family and friends, may help reduce the risk of dementia. The research examined how these activities, together with mental activities and the use of electronic devices, affected individuals with and without increased hereditary risk for dementia.

“Many studies have identified potential risk factors for dementia, but we wanted to know more about a wide variety of lifestyle habits and their potential role in the prevention of dementia,” said study author Huan Song, MD, Ph.D., of Sichuan University in Chengdu, China. “Our study found that exercise, household chores, and social visits were linked to a reduced risk of various types of dementia.”

The study involved 501,376 people from a UK database without dementia. The participants had an average age of 36.

The brain is an extremely complex organ whose exact functioning remains difficult to understand. On average, the human brain contains 100 billion neurons that fire upon receiving input signals from multiple sensory organs. But, what is truly remarkable about our brain is the synchronization of this neural firing when triggered by a common input. Put simply, common inputs can generate a collective response in neurons that are not only spatially separated but also have different firing characteristics.

The neural synchronization has been observed before in experiments, and is commonly demonstrated during rest and activities involving tasks. However, the common inputs which produce this are typically unknown in real-world situations. This raises an interesting question: is it possible to reconstruct this input by looking at the output of the neurons?

In a new study published in Physical Review E on September 12, 2022, a team of researchers from Japan, led by Professor Tohru Ikeguchi from Tokyo University of Science (TUS), set out to answer this question. The team, including Associate Professor Ryota Nomura of Waseda University (formerly TUS), and Associate Professor Kantaro Fujiwara of The University of Tokyo, looked at the firing rates of neurons and managed to reconstruct the input signal using a method called “superposed recurrence plot” (SRP).

Bluebird Bio Inc.’s gene therapy for a brain-wasting disease received accelerated approval from U.S. regulators, making it the first treatment of its kind for children living with cerebral adrenoleukodystrophy.