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The function of mRNA quality control in aging and age-related diseases

Aging is a complex biological process characterized by the gradual decline of physiological and molecular functions and increased susceptibility to age-associated diseases. Emerging evidence indicates the role of mRNA quality control mechanisms in the regulation of aging and longevity. This review focuses on the function of mRNA surveillance mechanisms, including nonsense-mediated mRNA decay (NMD), nonstop decay (NSD), and no-go decay (NGD), in aging and age-related diseases. We discuss the critical roles of these pathways in maintaining mRNA quality and preventing the accumulation of aberrant transcripts, which can contribute to aging and age-related disorders.

Scientists discover Alzheimer’s hidden “death switch” in the brain

Scientists have uncovered a hidden “death switch” in the brain that may be driving Alzheimer’s disease—and even found a way to turn it off in mice. The culprit is a toxic pairing of two proteins that, when combined, triggers the destruction of brain cells and fuels memory loss. By using a new compound to break apart this deadly duo, researchers were able to slow disease progression, protect brain cells, and even reduce hallmark amyloid buildup.

Dual immune response may keep HIV in check without medication

Imagine a game of chess where your opponent’s king is in check. It cannot move, but the game is not over—the piece remains on the board. This is how the body might control HIV on its own: The virus would be contained and unable to replicate or spread, but it would not have been eliminated. This is the goal of Professor Ole Schmeltz Søgaard and an international team of researchers—to enable more patients’ immune systems to keep the virus permanently in check without the need for daily medication. Their findings suggest that this requires two key components working in tandem: antibodies and T cells.

In a study published in Nature Immunology, the researchers followed patients who stopped taking their daily HIV medication after receiving experimental treatment. In a small group of patients, the virus has not returned.

“We can see that two branches of the immune system work together to control the virus. One targets one aspect of the virus, the other targets another. Together, they are effective enough to prevent the virus from escaping,” says Søgaard, Professor of Infectious Diseases at Aarhus University Hospital.

Johns Hopkins awarded $15M to develop platform to study neurological diseases, screen chemicals

The DROID platform will extend current in vitro approaches—test tubes and culture dishes—to modeling learning and memory using brain organoids, addressing a critical gap: Current in vitro assays cannot capture higher-order neural responses, and evaluations of neurotoxicity or drug efficacy still primarily rely on animal behavioral tests.

The researchers will also evaluate brain organoids derived from both healthy individuals and patients with Alzheimer’s disease and individuals with SYNGAP1-related disorders—a rare pediatric condition associated with intellectual disability, seizures, and autism—to test neural responses and sensitivity to pharmacological interventions.

By enabling researchers to assess complex neural responses that currently rely on animal behavioral tests, the DROIDp system aims to improve drug discovery and neurotoxicity testing. Ultimately, the goal of this platform is to provide a more predictive, human-relevant approach for studying neurological diseases and evaluating the safety of drugs and chemicals.

Abstract: A new mouse disease model for parkinsonism with psychiatric features 👇

https://doi.org/10.1172/JCI169297 Freja Herborg & team explore the behavioral consequences and dopaminergic dysfunction that arise from patient-derived mutations in the dopamine transporter associated with parkinsonism and co-morbid neuropsychiatric disease, establishing a new mouse disease model.

The images show striatal slices with decreased immunolabeling intensity of both DR1 and DR2 in DAT-I312F/D421N+/+ mice compared with WT mice.


1Molecular Neuropharmacology and Genetics Laboratory, Department of Neuroscience, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

2CNS Research Group, Department of Pharmacology and Physiology, Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montréal, Quebec, Canada.

3Centre for Neuroscience and Stereology, Copenhagen University Hospital Bispebjerg-Frederiksberg, Copenhagen, Denmark.

OMICmAge is a multiomic biological aging clock using electronic medical records

Using about 31,000 electronic medical records (EMRs), we developed the mortality biomarker EMRAge and used it to develop OMICmAge by integrating proteomic and metabolomic domains through epigenetic biomarker proxies. This scalable DNA-methylation measure quantifies biological aging, is associated with age-related incident and prevalent diseases, and its performance is comparable to or better than existing biomarkers at predicting mortality.

Age Reversal 2026: Why Getting Old Will Soon Be Optional

Is aging actually optional? According to this Harvard scientist, yes—and human trials start soon. He explains why aging is not inevitable but a medical condition we can now treat, sharing groundbreaking results from his lab including reversing blindness in animals and rejuvenating biological age by 75% in just six weeks.
The FDA has just approved the first human trials for age reversal, marking a turning point in medical history. This video covers the science, the economics, and a future where we spend our 80s and 90s as healthy as our 40s. This is the update you’ve been waiting for.
Credits to World Governments Summit & Dr David Sinclair

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