Scientists have made a groundbreaking discovery that could potentially reverse memory loss associated with neurodegenerative diseases. Researchers from Inserm and the University of Bordeaux, in collaboration with colleagues from the Université de Moncton in Canada, have successfully established a causal link between mitochondrial dysfunction and cognitive symptoms related to these conditions.

Mitochondria are tiny energy-producing structures within cells that provide the power needed for proper functioning. The brain is one of the most energy-demanding organs, relying on mitochondria to produce energy for neurons to communicate with each other. When mitochondrial activity is impaired, neurons fail to function correctly, leading to progressive neuronal degeneration and eventually, cell death.

In Alzheimer’s disease, for example, it has been observed that impaired mitochondrial activity precedes neuronal degeneration and ultimately, leads to memory loss. However, due to the lack of suitable tools, researchers were unable to determine whether mitochondrial alterations played a causal role in these conditions or were simply a consequence of the pathophysiological process.

In this pioneering study, researchers developed a unique tool that temporarily stimulates mitochondrial activity. By activating G proteins directly in mitochondria using an artificial receptor called mitoDreadd-Gs, they successfully restored both mitochondrial activity and memory performance in dementia mouse models.

“This work is the first to establish a cause-and-effect link between mitochondrial dysfunction and symptoms related to neurodegenerative diseases,” explains Giovanni Marsicano, Inserm research director. “Impaired mitochondrial activity could be at the origin of the onset of neuronal degeneration.”

The tool developed by researchers has opened doors to considering mitochondria as a new therapeutic target for treating memory loss associated with neurodegenerative diseases. Further studies are needed to measure the effects of continuous stimulation of mitochondrial activity and determine its potential impact on symptoms and neuronal loss.

Ultimately, this research holds promise for identifying molecular and cellular mechanisms responsible for dementia, facilitating the development of effective therapeutic targets, and potentially delaying or even preventing memory loss associated with neurodegenerative diseases.

The Lunar Trailblazer, a small satellite designed to map water on the Moon’s surface, ended its mission in July 2023. Despite extensive efforts by its operators, they were unable to establish two-way communications with the spacecraft after losing contact just one day after launch.

Lunar Trailblazer was launched on February 26 aboard a SpaceX Falcon 9 rocket from Kennedy Space Center in Florida. It shared a ride on the second Intuitive Machines robotic lunar lander mission, IM-2. The small satellite separated as planned from the rocket about 48 minutes after launch to begin its flight to the Moon.

Mission operators at Caltech’s IPAC established communications with the small spacecraft at 8:13 p.m. EST. Contact was lost the next day. Without two-way communications, the team was unable to fully diagnose the spacecraft or perform the thruster operations needed to keep Lunar Trailblazer on its flight path.

“At NASA, we undertake high-risk, high-reward missions like Lunar Trailblazer to find revolutionary ways of doing new science,” said Nicky Fox, associate administrator, Science Mission Directorate at NASA Headquarters in Washington. “While it was not the outcome we had hoped for, mission experiences like Lunar Trailblazer help us to learn and reduce the risk for future, low-cost small satellites to do innovative science as we prepare for a sustained human presence on the Moon.”

The limited data the mission team had received from Lunar Trailblazer indicated that the spacecraft’s solar arrays were not properly oriented toward the Sun, which caused its batteries to become depleted. For several months, collaborating organizations around the world listened for the spacecraft’s radio signal and tracked its position.

Ground radar and optical observations indicated that Lunar Trailblazer was in a slow spin as it headed farther into deep space. “As Lunar Trailblazer drifted far beyond the Moon, our models showed that the solar panels might receive more sunlight, perhaps charging the spacecraft’s batteries to a point it could turn on its radio,” said Andrew Klesh, Lunar Trailblazer’s project systems engineer at NASA’s Jet Propulsion Laboratory in Southern California.

However, as time passed, Lunar Trailblazer became too distant to recover. Its telecommunications signals would have been too weak for the mission to receive telemetry and to command. Despite this setback, the technology developed for the mission will live on in future projects.

The High-resolution Volatiles and Minerals Moon Mapper (HVM3) imaging spectrometer was built by JPL to detect and map the locations of water and minerals. The Lunar Thermal Mapper (LTM) instrument was built by the University of Oxford in the United Kingdom and funded by the UK Space Agency to gather temperature data and determine the composition of silicate rocks and soils.

The collective knowledge and technology developed for Lunar Trailblazer will cross-pollinate to other projects as the planetary science community continues work to better understand the Moon’s water. Some of that technology will live on in the JPL-built Ultra Compact Imaging Spectrometer for the Moon (UCIS-Moon) instrument that NASA recently selected for a future orbital flight opportunity.

Lunar Trailblazer was selected by NASA’s SIMPLEx (Small Innovative Missions for Planetary Exploration) competition, which provides opportunities for low-cost science spacecraft to ride-share with selected primary missions. To maintain the lower overall cost, SIMPLEx missions have a higher risk posture and less-stringent requirements for oversight and management.

This higher risk acceptance bolsters NASA’s portfolio of targeted science missions designed to test pioneering mission approaches. Caltech, which manages JPL for NASA, led Lunar Trailblazer’s science investigation, and Caltech’s IPAC led mission operations.

Along with managing Lunar Trailblazer, NASA JPL provided system engineering, mission assurance, the HVM3 instrument, and mission design and navigation. Lockheed Martin Space provided the spacecraft, integrated the flight system, and supported operations under contract with Caltech. The University of Oxford developed and provided the LTM instrument, funded by the UK Space Agency.

Lunar Trailblazer, a project of NASA’s Lunar Discovery and Exploration Program, was managed by NASA’s Planetary Missions Program Office at Marshall Space Flight Center in Huntsville, Alabama, for the agency’s Science Mission Directorate in Washington.

In a groundbreaking study, researchers at Mayo Clinic have discovered that a sugar molecule used by cancer cells to evade the immune system could also help treat type 1 diabetes. The team, led by immunology researcher Virginia Shapiro, Ph.D., found that dressing up beta cells with the same sugar molecule, known as sialic acid, enabled the immune system to tolerate them.

Type 1 diabetes is a chronic autoimmune condition in which the immune system mistakenly attacks pancreatic beta cells that produce insulin. This leads to an estimated 1.3 million people in the U.S. suffering from the disease. In their studies, Shapiro’s team used a cancer mechanism and turned it on its head by applying it to type 1 diabetes.

The researchers took a closer look at a preclinical model of type 1 diabetes and found that beta cells engineered to produce an enzyme called ST8Sia6, which increases sialic acid on the surface of tumor cells, were not attacked by the immune system. In fact, they were 90% effective in preventing the development of type 1 diabetes.

The team’s findings show that it is possible to engineer beta cells that do not prompt an immune response. This breakthrough has the potential to improve therapy for patients with type 1 diabetes, who currently rely on synthetic insulin or transplantation of pancreatic islet cells with immunosuppression.

Dr. Shapiro aims to explore using the engineered beta cells in transplantable islet cells without the need for immunosuppression. While still in the early stages, this study may be one step toward improving care for patients with type 1 diabetes.