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Molecular mechanisms show how the blood-brain barrier gets leakier with age

A new study from researchers at the University of Illinois Chicago reveals how the blood-brain barrier gets leakier with age, contributing to memory deficits. The study, published in Cell Reports, uncovered the molecular mechanisms behind this process and could provide new therapeutic targets to address cognitive decline earlier in the aging process.

The is a layer of cells lining the brain’s blood vessels that keep viruses, bacteria and toxins out while allowing helpful nutrients and chemicals in. A key structure of the blood-brain barrier are tight junctions that act as bridges between cells, restricting entry of molecules. A protein called occludin helps fulfill this essential role.

“It’s a highly regulatable process that allows some molecules to go through and others to remain in circulation,” said Yulia Komarova, UIC associate professor in the department of pharmacology and at the College of Medicine and senior author of the study. “Basically, it’s a mechanism that separates the central nervous system from everything else.”

Vitamin D supplements may slow biological aging

Results from a randomized controlled trial reveal that vitamin D supplementation helps maintain telomeres, protective caps at the ends of chromosomes that shorten during aging and are linked to the development of certain diseases.

The new report, which is published in The American Journal of Clinical Nutrition, is based on data from a VITAL (VITamin D and OmegA-3 TriaL) sub-study co-led by researchers at the Harvard-affiliated Mass General Brigham and the Medical College of Georgia, and supports a promising role in slowing a pathway for biological aging.

“VITAL is the first large-scale and long-term randomized trial to show that vitamin D supplements protect telomeres and preserve telomere length,” said co-author JoAnn Manson, the principal investigator of VITAL and chief of the Division of Preventive Medicine at Harvard-affiliated Brigham and Women’s Hospital and the Michael and Lee Bell Professor of Women’s Health at Harvard Medical School.


Trial shows protection against telomere shortening, which heightens disease risk.

Adult Neurogenesis: Beyond Rats and Mice

Basically I believe that the flatworm could give the genetic code for essentially brain immortality other just nad plus. But it would have to be made in the brain and controlled possibly with nanotransfection which would scan the body and modify the human brain cells to have its characteristics that may already exist in the human brain also.


Powerful genetic tools in classical laboratory models have been fundamental to our understanding of how stem cells give rise to complex neural tissues during embryonic development. In contrast, adult neurogenesis in our model systems, if present, is typically constrained to one or a few zones of the adult brain to produce a limited subset of neurons leading to the dogma that the brain is primarily fixed post-development. The freshwater planarian (flatworm) is an invertebrate model system that challenges this dogma. The planarian possesses a brain containing several thousand neurons with very high rates of cell turnover (homeostasis), which can also be fully regenerated de novo from injury in just 7 days. Both homeostasis and regeneration depend on the activity of a large population of adult stem cells, called neoblasts, throughout the planarian body. Thus, much effort has been put forth to understand how the flatworm can continually give rise to the diversity of cell types found in the adult brain. Here we focus on work using single-cell genomics and functional analyses to unravel the cellular hierarchies from stem cell to neuron. In addition, we will review what is known about how planarians utilize developmental signaling to maintain proper tissue patterning, homeostasis, and cell-type diversity in their brains. Together, planarians are a powerful emerging model system to study the dynamics of adult neurogenesis and regeneration.

The adult brain has long been thought to be a fixed structure due to its immense complexity as is illustrated succinctly in the following quote from prominent nineteenth century neuroscientist and Nobel laureate Santiago Ramón y Cajal:

“Once the development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. In the adult centers, the nerve paths are something fixed, ended, and immutable. Everything may die, nothing may be regenerated. It is for the science of the future to change, if possible, this harsh decree.”

Without Gene Therapies it Will Not be Possible to Extend Life | 071 Liz Parrish, Mba

Dr. Esra Çavuşoğlu, PhD’s 71st Ayık Kafa podcast guest is Liz Parrish explores the transformative potential of gene therapy in extending human longevity and enhancing healthspan.

Liz Parrish MBA, is the Founder and CEO of BioViva Sciences USA Inc. BioViva is committed to extending healthy lifespans using gene therapy and works on combinatorial gene therapies with its proprietary CMV gene therapy delivery platform.

Liz is a humanitarian, entrepreneur, author, and innovator. In addition, she is a proponent of the Best Choice Medicine plan (BCM), a more efficient and streamlined regulatory model around the use of genetic therapies.

She shares her personal journey, the scientific basis for gene therapy, and the economic implications of aging-related diseases. The podcast also takes a closer look at the four different gene therapies that Liz Parrish administered to herself: Klotho, Follistatin, PGC-1α, and Telomerase Reverse Transcriptase. The discussion covers the various gene therapies being developed, their safety, ethical considerations, and the importance of early intervention. Liz emphasizes the need for public awareness and investment in longevity research to make these therapies accessible to all.

#EsraÇavuşoğlu #AyıkKafa #ElevatingLifeEvolvingHealth #Longevilab #LizParrish #Longevity #genetherapy.

Liz Parrish:

The Cerebral Cortex Ages Less than Thought

The human cerebral cortex is only a few millimetres thick and arranged in numerous folds. This tissue usually becomes thinner with age. “This is a hallmark of aging. It is attributed, among other things, to the loss of neurons. As a result, some abilities deteriorate. In any case, it is generally assumed that less brain volume means reduced function,” explains Prof. Esther Kühn, a neuroscientist at DZNE and the Hertie Institute for Clinical Brain Research. “However, little is known about how exactly the cortex actually ages. This is remarkable, given that many of our daily activities depend on a functioning cortex. That’s why we examined the situation with high-resolution brain scans.”

Together with colleagues from Tübingen and Magdeburg, Esther Kühn focused on a part of the cerebral cortex where signals from the tactile sense are processed. This “primary somatosensory cortex” is located on the left and right side of the top of the head and extends along a strip about a finger’s width wide towards each ear. “This brain area is relevant for the perception of one’s own body and for interacting with the environment,” explains the neuroscientist. “When I pick up a key, grasp a door handle or even walk, I constantly need haptic feedback to control my movements. The corresponding stimuli converge in this area and are also processed here”

Using magnetic resonance imaging (MRI), the researchers were able to map this area of the cerebral cortex with unprecedented accuracy. To do this, they employed a particularly sensitive scanner with a magnetic field strength of seven Tesla, enabling them to image minute brain structures about the size of a grain of sand. A total of around 60 women and men between the ages of 21 and 80 were examined. “Until now, it had not been considered that the primary somatosensory cortex consists of a stack of several extremely thin layers of tissue, each with its own architecture and function. We have now found that these layers age differently. Although the cerebral cortex becomes thinner overall, some of its layers remain stable or, surprisingly, are even thicker with age. Presumably because they are particularly solicited and thus retain their functionality. We therefore see evidence for neuroplasticity, that is, adaptability, even in senior people.”

David Furman: How Microgravity Accelerates Aging & What It Teaches Us About Longevity | LSD 2025

In this Longevity Summit Dublin 2025 talk, Dr. David Furman (Buck Institute for Research on Aging) reveals how space medicine is becoming a powerful model for studying accelerated aging. From NASA collaborations to organoid experiments in simulated microgravity, Dr. Furman shows how heart, brain, and immune organoids age up to 10 years in just 24 hours — and how this can accelerate drug discovery for neurodegeneration, cardiovascular disease, and immune decline. Learn how microgravity research can predict your biological future and identify interventions to slow or reverse aging.

Chapters:
00:00 Introduction & NASA collaboration.
01:25 Accelerated aging in astronauts.
03:02 Simulating microgravity with organoids.
05:16 Brain, heart & immune system aging signatures.
07:03 Biological age clocks in organoids.
09:22 Parkinson’s, cardiomyopathy & immune dysfunction findings.
11:56 Translating microgravity science into longevity medicine.
13:43 Predicting future aging trajectories.
15:34 Beyond Age – a clinical test for aging projection.
16:17 Closing remarks.

#LongevityScience #AgingResearch #Microgravity #SpaceMedicine #BiologicalAge #LongevitySummit

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