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Researchers at the Allen Institute have identified a specific brain region in mice where aging triggers significant changes in numerous cell types. The study also pinpointed which cell types undergo the most profound transformations.

This new information, published in the journal Nature, points toward potential approaches for slowing or controlling the aging process in the brain.

The research was focused on numerous glial cell types – the brain’s “support cells” – that demonstrated considerable shifts in gene activity with age. Among the cells most affected were microglia, border-associated macrophages, oligodendrocytes, tanycytes, and ependymal cells.

“The ultimate goal is to extend healthspan—meaning the number of years aging adults live healthy lives and enjoy overall well-being by compressing the frailty and disability that comes with aging into a shorter duration of time near the end of life,” says Andrew Brack, PhD, the PROSPR Program Manager.

The new venture will be building on some of the work that the National Institute of Aging (NIH) has been working on and will be working in collaboration with various organizations in the biotechnology industry as well as some unspecified regulators to accelerate the development, testing, and availability of new therapeutic that targets human healthspan.

It is hoped that the new initiative, along with positively impacting the healthspan of Americans, will also help to enhance the economy across the nation.

Largest brain aging study points to possible connections between diet, inflammation, and brain health.

Scientists at the Allen Institute have discovered specific types of brain cells in mice that experience significant changes as they age. They also identified a distinct “hotspot” where many of these changes are concentrated. Published today (January 1) in Nature, these findings could lead to the development of therapies aimed at slowing or managing the brain’s aging process.

Sensitive cells: Scientists discovered dozens of specific cell types, mostly glial cells, known as brain support cells, that underwent significant gene expression changes with age. Those strongly affected included microglia and border-associated macrophages, oligodendrocytes, tanycytes, and ependymal cells.

Inflammation and neuron protection: In aging brains, genes associated with inflammation increased in activity while those related to neuronal structure and function decreased.

Aging hot spot: Scientists discovered a specific hot spot combining both the decrease in neuronal function and the increase in inflammation in the hypothalamus. The most significant gene expression changes were found in cell types near the third ventricle of the hypothalamus, including tanycytes, ependymal cells, and neurons known for their role in food intake, energy homeostasis, metabolism, and how our bodies use nutrients. This points to a possible connection between diet, lifestyle factors, brain aging, and changes that can influence our susceptibility to age-related brain disorders.

Brain-wide cell-type-specific transcriptomic signatures of healthy ageing in mice.


Scientists at the Allen Institute have identified specific cell types in the brain of mice that undergo major changes as they age, along with a specific hot spot where many of those changes occur. The discoveries, published in the journal Nature, could pave the way for future therapies to slow or manage the aging process in the brain.

The scientists discovered dozens of specific cell types, mostly , known as brain support cells, that underwent significant gene expression changes with age. Those strongly affected included microglia and border-associated macrophages, oligodendrocytes, tanycytes, and ependymal cells.

They found that in aging brains, genes associated with inflammation increased in activity while those related to neuronal structure and function decreased.

Researchers have developed a method to direct stem cells to form specific structures. By triggering the expression of specific genes in mouse embryonic stem cells, synthetic organizer cells were created, which can assemble in specific ways and carry out various phsyiological functions. This work is an important step on the road to eventually using synthetic cells to repair damaged tissues or regenerate organs. The research has been reported in Cell.

The researchers created synthetic organizer cells that could generate a structure like a mouse body, from head to tail, that underwent processes that were similar to those in mouse embryonic development. Another type of synthetic organizer cell was used to produce a structure that was similar to a heart, and featured a central chamber. This synthetic, heart-like structure also had a network of blood vessels and beat regularly.

New research identifies E-TCmito as a key link between neuronal activity and mitochondrial function, highlighting its potential to address cognitive decline in aging and diseases like Alzheimer’s.

New research in mice has identified a critical mechanism that connects neuronal activity with mitochondrial function, offering insight into potential strategies to address age-related cognitive decline. Mitochondria, essential for meeting the energy needs of active neurons, generate adenosine triphosphate (ATP) primarily through oxidative phosphorylation (OXPHOS).

As mammals age, the efficiency of mitochondrial metabolism in the brain declines, significantly impacting neuronal and network function. The disruption of the OXPHOS pathway contributes to oxidative stress and mitochondrial dysfunction, exacerbating these challenges.

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