Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: biotech/medical – Page 549

Synaptic Dysfunction in Dementia Can Be Modelled in Patient-Derived Neurons

Neurons produced from frontotemporal dementia patients’ skin biopsies using modern stem cell technology recapitulate the synaptic loss and dysfunction detected in the patients’ brains, a new study from the University of Eastern Finland shows.

Frontotemporal dementia is a progressive neurodegenerative disease affecting the frontal and temporal lobes of the brain. The most common symptoms are behavioral changes, difficulties in understanding or producing speech, problems in movement, and psychiatric symptoms. Often, frontotemporal dementia has no identified genetic cause, but especially in Finnish patients, hexanucleotide repeat expansion in the C9orf72 gene is a common genetic cause, present in about half of the familial cases and in 20 per cent of the sporadic cases where there is no family history of the disease. However, the disease mechanisms of the different forms of frontotemporal dementia are still poorly understood, and there are currently no effective diagnostic tests or treatments affecting the progression of the disease in clinical use.

Brain imaging and neurophysiological studies have shown that pathological and functional changes underlying the symptoms occur at synapses, the connections between brain neurons, in frontotemporal dementia patients. PET imaging studies have shown significant synapse loss in the brain, and transcranial magnetic stimulation, on the other hand, has indicated disturbed function of both excitatory and inhibitory neurotransmitter systems, leading to deficient neurotransmission. Often, drugs affecting the different neurotransmitter systems are used to mitigate the symptoms of frontotemporal dementia patients.

Chinese medicine extract tetrandrine’s precise mechanism of action opens new avenues for drug discovery

With this discovery, the researchers propose that tetrandrine can be used to disrupt processes critical to the survival and replication of viruses, such as Ebola and COVID-19, by targeting LIMP-2 to alter lysosomal calcium release.

Importantly, these findings highlight lysosome-related mechanisms as a new frontier for , offering novel strategies for treating diseases caused by calcium imbalance, including neurodegenerative disorders like Alzheimer’s and Parkinson’s, as well as certain metastatic cancers.

Prof. Ko said, “This is the first time a function of LIMP-2 in calcium signaling has been uncovered. From a cell biology perspective, our study has revealed a completely new pathway for NAADP-regulated calcium signaling, through LIMP-2 and sphingosine. From an anti-viral treatment perspective, the study has identified LIMP-2 as a key target of tetrandrine for the treatment of Ebola virus infection, with broader applications in other antiviral therapies.”

MIT and Harvard Build “Invisible” Immune Cells That Obliterate Cancer

MIT and Harvard scientists have created engineered CAR-NK cells that can hide from the immune system and more effectively destroy cancer.

The cells are designed to suppress immune-rejection signals and enhance tumor-killing power. Tested in humanized mice, they wiped out cancer while avoiding dangerous immune reactions.

A major breakthrough in immune engineering.

It’s all in your head: Select neurons in the brainstem may hold the key to treating chronic pain

Acute or short-lived pain, despite its bad reputation, is usually a lifesaver. It acts as a transient negative sensory experience that helps us avoid danger. Touch a hot stove, stub a toe, or bonk your head on a low branch, and the nervous system cues up an “Ow!” Over time, the sting fades, the wound heals, but the lesson sticks.

Chronic pain is different; the alarm keeps blaring long after the fire is out, and then the pain itself becomes the problem. Nearly 50 million people in the United States live with , an invisible and often untreatable condition that can linger for decades. “It’s not just an injury that won’t heal,” says neuroscientist at the University of Pennsylvania J. Nicholas Betley, “it’s a brain input that’s become sensitized and hyperactive, and determining how to quiet that input could lead to better treatments.”

Now, research led by Betley and collaborators at the University of Pittsburgh and Scripps Research Institute has identified a key to regulating long-term pain states: a group of cells called Y1 receptor (Y1R)-expressing in the brainstem’s lateral (lPBN). These neurons are activated during enduring pain states, but they also integrate information about hunger, fear and thirst, allowing for to be modulated by other signaling more urgent needs.

1,000-year-old gut microbiome revealed for young man who lived in pre-Hispanic Mexico

Analysis of preserved feces and intestinal tissue has revealed specific types of bacteria that were present in the microbiome of a young adult man who lived in Mexico about 1,000 years ago, prior to Spanish colonization. Santiago Rosas-Plaza of Universidad Nacional Autónoma de México and colleagues present these findings in PLOS One.

The consists of microorganisms, including , that naturally live in people’s intestines. Certain types of bacteria are widely associated with the human gut microbiome, but a person’s particular mix of bacteria may vary depending on factors such as age, diet, health, and where they live. Studying ancient microbiomes using mummies and can therefore deepen understanding of ancient populations and show how the human microbiome may have changed over time.

A growing number of ancient microbiomes have been revealed, including for an ancient Incan person and Germany’s “Tyrolean Iceman.” To further expand the field, Rosas-Plaza and colleagues analyzed the exceptionally well-preserved remains of a man discovered in a in Zimapán, Mexico. Prior analyses suggest the “Zimapán man” was most likely a seasonal seminomadic hunter-gatherer who was part of the ancient Mesoamerican Otopame culture and died about 1,000 years ago between the ages of 21 and 35.

‘Traffic controller’ protein that protects DNA discovered, and it may help kill cancer cells

Mayo Clinic researchers have identified a protein that acts like a traffic controller for DNA, preventing damage during cell division—a discovery that could lead to new cancer therapies, according to a study published in Nature.

“DNA is the code of life. It’s critical for how a cell functions, but it’s also critical for our own being and defines what we are,” says Zhenkun Lou, Ph.D., the Swanson/Schmucker Endowed Professor to Support Health and Cancer Research at Mayo Clinic and the senior author of the new study.

When cells divide, DNA must be copied from one cell to the next—a process called replication. Dr. Lou’s research team discovered that a protein called KCTD10 plays a surprising role in protecting DNA during this critical stage. Acting like a built-in sensor, KCTD10 helps shield the DNA replication from damage.

Alzheimer’s disease research in brain tissue from African American donors points to roles for many novel genes

The prevalence of Alzheimer’s disease (AD) is approximately two times higher in African Americans (AA) compared to white/European-ancestry (EA) individuals living in the U.S. Some of this is due to social determinants of health such as disparities in health care access and quality of education, biases in testing and higher rates of AD risk factors such as cardiovascular disease and diabetes in those who identify as African American.

Although many studies have examined differences in (a measure of the amount of protein encoded by a gene) in from AD cases and controls in EA or mixed ancestry cohorts, the number of AA individuals in these studies was unspecified or too small to identify significant findings within this group alone.

In the largest AD study conducted in brain tissue from AA donors, researchers from Boston University Chobanian & Avedisian School of Medicine have identified many genes, a large portion of which had not previously been implicated in AD by other , to be significantly more or less active in tissue from AD cases compared to controls. The most notable finding was a 1.5 fold higher level of expression of the ADAMTS2 gene in brain tissue from those with autopsy-confirmed AD.

Engineered CAR-NK cells could evade immune rejection and target cancer more effectively

One of the newest weapons that scientists have developed against cancer is a type of engineered immune cell known as CAR-NK (natural killer) cells. Similar to CAR-T cells, these cells can be programmed to attack cancer cells.

MIT and Harvard Medical School researchers have now come up with a new way to engineer CAR-NK cells that makes them much less likely to be rejected by the patient’s , which is a common drawback of this type of treatment.

The new advance may also make it easier to develop “off-the-shelf” CAR-NK cells that could be given to patients as soon as they are diagnosed. Traditional approaches to engineering CAR-NK or CAR-T cells usually take several weeks.

/* */