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Category: biotech/medical – Page 4

This nasal spray rewinds the aging brain, restoring memory and reversing inflammation in preclinical models

Picture this: your brain is a high-performance engine. Over decades, it doesn’t just wear down, it also starts to run hot. Tiny “fires” of inflammation smolder deep within the brain’s memory center, creating a persistent brain fog that makes it harder to think, form new memories or even adapt to new environments, all the while increasing the risk to disorders like Alzheimer’s disease.

Scientists call this slow burn “neuroinflammaging,” and for decades it was thought to be the inevitable price of growing older. Until now.

A landmark study by researchers at Texas A&M University Naresh K. Vashisht College of Medicine suggests the inflammatory tide responsible for brain aging and brain fog might actually be reversible. And the solution doesn’t involve brain surgery, but a simple nasal spray.

Perovskite Nanocrystals, Quantum Dots, and Two-Dimensional Structures: Synthesis, Optoelectronics, Quantum Technologies, and Biomedical Imaging

💬Editorial: Decade-long follow-up highlights that patients with surgically treated ChronicSubduralHematoma have persistent excess mortality and long-term cognitive and functional impairment, even when overall quality of life appears preserved.

In the setting of aging populations and rising antithrombotic use, chronic subdural hematomas (cSDH) are increasingly common in high-income countries. While discussed in the medical literature for centuries,1 clinical research on cSDH in the modern era initially focused on surgical approaches and the risk of short-term mortality and recurrence.2-4 In this setting, cSDH was perceived to be a relatively benign disease; however, recent work has challenged this reputation. Patients with cSDH have persistently elevated long-term mortality when compared with controls,5 and those who survive are often left with functional and cognitive impairment.6 Unfortunately, most prior studies of long-term outcomes were small or had limited data on premorbid health, and none had data on functional status or quality of life.

In this issue of JAMA Neurol ogy, Petutschnigg et al7 expand on this work by examining mortality, function, and quality of life 10 years after surgical management of cSDH. To achieve this, they used patients who had previously been enrolled in a cSDH clinical trial from 2012 through 2016, which was conducted at a single center in Switzerland and examined the use of routine follow-up computed tomography scans in surgically managed patients with cSDH. The study authors obtained all-cause mortality for all 359 participants through 2023 using a nationwide data source. Each patient was then matched by age, sex, and birth month to controls from the Swiss population. Then, they obtained health-related quality of life by administering a validated survey to consenting participants, getting a response in 147 of 202 survivors at a mean of 10.55 years from the cSDH. Results from these participants were compared with normative values for a European population, using standardized age and sex strata.

The authors7 found a significantly higher mortality rate among patients with cSDH when compared with controls, with the absolute risk difference widening from 6% at 1 year to 18% at 10 years. Among those who survived, both men and women showed significant impairment in cognitive and role functioning (ie, how much their daily work/hobbies are impaired) when compared with normative controls. In addition, men (but not women) showed significant additional impairment in physical functioning and social functioning when compared with normative controls. Importantly, perceived quality of life was not reduced in either men or women. Discordance between functional impairments and perceived quality of life has been observed in other types of brain injury, a phenomenon termed the disability paradox,8 and should similarly caution against therapeutic nihilism when it comes to patients with cSDH.

Scientists Grow Electronics Inside the Brains of Living Mice

Yet most implants require extensive surgery and risk damaging the brain’s delicate tissue. The new technology would avoid these downsides by building electrodes directly at the target.

“Our work points to a future where doctors could ‘grow’ soft, wire-free electronic interfaces inside the brain using the patient’s own blood, then gently dial brain activity up or down from outside the head using harmless near-infrared light,” study author Krishna Jayant said in a press release.

The brain produces every one of our sensations, movements, emotions, and decisions. Scientists have long sought to decode and manipulate its activity with a range of hardware.

Nociceptive neurons protect cancer cells against oxidative stress

How cancer cells exploit the tumor microenvironment to alleviate oxidative stress remains largely unclear. Zhang et al. find that nociceptive neurons, via secretion of EREG, protect HNSCC against oxidative stress-induced cell death. Targeting nociceptive neurons improves the therapeutic efficacy of chemotherapies, including cisplatin.

Targeting KRAS G12C Mutation in Colorectal Cancer, A Review: New Arrows in the Quiver

Kirsten rat sarcoma virus oncogene homolog (KRAS) is the most frequently mutated oncogene in human cancer. In colorectal cancer (CRC), KRAS mutations are present in more than 50% of cases, and the KRAS glycine-to-cysteine mutation at codon 12 (KRAS G12C) occurs in up to 4% of patients. This mutation is associated with short responses to standard chemotherapy and worse overall survival compared to non-G12C mutations. In recent years, several KRAS G12C inhibitors have demonstrated clinical activity, although all patients eventually progressed. The identification of negative feedback through the EGFR receptor has led to the development of KRAS inhibitors plus an anti-EGFR combination, thus boosting antitumor activity. Currently, several KRAS G12C inhibitors are under development, and results from phase I and phase II clinical trials are promising.

Frontiers: As a significant mental health disorder worldwide

The treatment of depression has long faced the challenges of a low treatment rate, significant drug side effects and a high relapse rate. Recent studies have revealed that the gut microbiota and neuronal mitochondrial dysfunction play central roles in the pathogenesis of depression: the gut microbiota influences the course of depression through multiple pathways, including immune regulation, HPA axis modulation and neurotransmitter metabolism. Mitochondrial function serves as a key hub that mediates mood disorders through mechanisms such as defective energy metabolism, impaired neuroplasticity and amplified neuroinflammation. Notably, a bidirectional regulatory network exists between the gut microbiota and mitochondria: the flora metabolite butyrate enhances mitochondrial biosynthesis through activation of the AMPK–PGC1α pathway, whereas reactive oxygen species produced by mitochondria counteract the flora composition by altering the intestinal epithelial microenvironment. In this study, we systematically revealed the potential pathways by which the gut microbiota improves neuronal mitochondrial function by regulating neurotransmitter synthesis, mitochondrial autophagy, and oxidative stress homeostasis and proposed the integration of probiotic supplementation, dietary fiber intervention, and fecal microbial transplantation to remodel the flora–mitochondrial axis, which provides a theoretical basis for the development of novel antidepressant therapies targeting gut–brain interactions.

Depression is a disorder that severely affects the mental health of the global population and is characterized by persistent low mood, loss of interest and cognitive dysfunction (GBD 2017 Disease and Injury Incidence and Prevalence Collaborators, 2018; COVID-19 Mental Disorders Collaborators, 2021; Salari et al., 2020). Globally, depression is one of the leading causes of mental disability. According to the World Health Organization (WHO), the global prevalence of depression is approximately 4.4%, which means that more than 300 million people worldwide suffer from depression (Xu et al., 2024). In addition, depression is one of the major causes of suicide deaths, with nearly 800,000 people worldwide dying by suicide each year (World Health Organization, 2021).

How multiple sclerosis kills neurons

MS is typically diagnosed when clinicians see lesions in the myelin-rich white matter of the brain on MRI scans. White matter is made of the nerves that link brain cells and it looks white on a brain scan.

The brain’s grey matter, which houses the “bodies” of the brain cells, can also have MS lesions, especially in its outer layers. These lesions are less common — and harder to see on a brain scan — but they are a sign of chronic and disabling MS.

The scientists wanted to learn more about the neurons that died in these grey-matter lesions, which express a gene called CUX2. In the first study, they looked at developing mouse brains to see how CUX2 neurons are born. This occurs early in life, when the brain is growing quickly, putting cells under tremendous stress.

The cells relied on a mechanism to repair their DNA as they rapidly multiplied, fanned out into the far reaches of the brain and wired up with one another. The mechanism depends on a stress-response gene called ATF4 to keep chromosomes intact. When the team removed ATF4, the growing neurons were rife with DNA damage, and this prevented the frontal part of the brain from forming.

In the second study, the team found DNA damage in grey matter lesions from people with MS involving the same neurons.

In mouse models of MS, the researchers saw that inflammation sparked chemical reactions that damaged DNA in CUX2 neurons. The repair systems that protect these neurons from the stresses of development could no longer keep up; and this led to brain damage.

Together, the two studies outline the natural way the brain’s outer layer neurons cope with DNA damage — and how that system breaks down in MS. ScienceMission sciencenewshighlights.

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