This year quietly rewired how researchers think about aging, what truly predicts long-term health, and which biohacking ideas deserve serious attention versus skepticism. From brain aging to muscle strength, from AI-driven drug discovery to cooling hype around supplements, 2025 redrew the map of healthspan science.
Here’s the clear-eyed recap of what actually mattered.
A study by the Mildred Scheel Early Career Center group led by Dr. Mohamed Elgendy at the TUD Faculty of Medicine provides fundamental insights into cancer biology. Published in Nature Communications, the study shows for the first time that the protein MCL1 not only inhibits programmed cell death, but also plays a central role in tumor metabolism.
The researchers have succeeded in tracing two classic hallmarks of cancer—the evasion of apoptosis (a form of programmed cell death) and the dysregulation of energy metabolism—back to a common molecular mechanism.
The study focuses on the protein MCL1, which is strongly overexpressed in many tumor types and has previously been considered primarily an anti-apoptotic factor of the Bcl-2 protein family.
One of the main proteins that contributes to Alzheimer’s disease is called phospho-tau (p-tau). When p-tau gets too many phosphate groups attached to it (a process called hyperphosphorylation), it starts to stick together and form clumps called “tangles” inside of brain nerve cells.
A new study by Mass General Brigham investigators shows that tau hyperphosphorylation may be a consequence of an antiviral response that protects the brain from infection. Results are published in Nature Neuroscience.
“As a geneticist, I always wondered why humans had evolved gene mutations predisposing to Alzheimer’s disease,” said senior author Rudolph Tanzi, Ph.D., Director of the McCance Center for Brain Health and Genetics and Aging Research Unit in the Mass General Brigham Department of Neurology.
Small cell lung cancer (SCLC) is one of the most aggressive forms of lung cancer, with a five-year survival rate of only 5%. Despite this poor prognosis, SCLC is initially highly responsive to chemotherapy. However, patients typically relapse and experience very rapid disease progression. Current research into the biological mechanisms behind SCLC remains essential in order to prolong treatment responses, overcome relapse and, ultimately, improve long-term patient outcomes.
A research team led by Professor Dr. Silvia von Karstedt (Translational Genomics, CECAD Cluster of Excellence on Aging Research, and Center for Molecular Medicine Cologne—CMMC) has discovered a novel mechanism used by this type of cancer that helps explain its aggressive nature. The study titled “Lack of Caspase 8 Directs Neuronal Progenitor-like reprogramming and Small Cell Lung Cancer Progression” is published in Nature Communications.
Science Signaling retracted a 2017 paper that linked a specific amyloid form (amyloid-beta 56) to tau pathology after an investigation into allegations of data manipulation. Author Sylvain Lesné, PhD, who resigned from the University of Minnesota earlier this year, objected to the retraction.
Older adults who were awake more during the night performed worse on cognitive tests no matter how long they slept, data from the Einstein Aging Study showed. (Sleep Health)
Human herpesvirus 7 could be a contributing factor in multiple sclerosis (MS) etiology, a case-control study in Sweden suggested. (Brain Communications)
— News and commentary from the world of neurology and neuroscience.
Despite risks, results from both trials highlight the promise of one-and-done CAR T therapy for deadly blood cancers. But it’s still early days. Scientists need to carefully follow patients over years to understand how long upgraded T cells remain in the body and their effect on cancers.
And not all viral carriers are made the same. Lentiviruses, used in both studies, can tunnel into the human genome, causing DNA typos that potentially trigger secondary cancers. The durability of the therapy, its longevity, and immune side effects also need to be studied.
Kelonia is adding more patients to their trial, amid an increasingly competitive landscape. AstraZeneca has acquired EsoBiotec to bring its technology to market. AbbVie, a drug company in Illinois, is testing the delivery of gene-editing tools to T cells via fatty nanoparticles in clinical trials. And Kelonia is planning a second clinical trial with an initial 20 patients and 20 more in an expansion phase, none of whom responded to at least three previous treatments.
Research exploring the impact of development and aging on working memory (WM) has primarily concentrated on visual and verbal domains, with limited attention paid to the tactile modality. The current study sought to evaluate WM encompassing storage and manipulation across these three modalities, spanning from childhood to old age. The study included 134 participants, divided into four age groups: 7–8, 11–12, 25–35, and 60–69. Each participant completed the Visuospatial Span, Digit Span, and Tactual Span, with forward and backward recall. The findings demonstrated a consistent trend in both forward and backward stages. Performance improved until young adulthood, progressively diminishing with advancing age. In the forward stage, the Tactual Span performance was worse than that of the Digit and Visuospatial Span for all participants.
At more than 200 years, the maximum lifespan of the bowhead whale exceeds that of all other mammals. The bowhead is also the second-largest animal on Earth1, reaching over 80,000 kg. Despite its very large number of cells and long lifespan, the bowhead is not highly cancer-prone, an incongruity termed Peto’s paradox2.
Here, to understand the mechanisms that underlie the cancer resistance of the bowhead whale, we examined the number of oncogenic hits required for malignant transformation of whale primary fibroblasts. Unexpectedly, bowhead whale fibroblasts required fewer oncogenic hits to undergo malignant transformation than human fibroblasts. However, bowhead whale cells exhibited enhanced DNA double-strand break repair capacity and fidelity, and lower mutation rates than cells of other mammals. We found the cold-inducible RNA-binding protein CIRBP to be highly expressed in bowhead fibroblasts and tissues.
Bowhead whale CIRBP enhanced both non-homologous end joining and homologous recombination repair in human cells, reduced micronuclei formation, promoted DNA end protection, and stimulated end joining in vitro. CIRBP overexpression in Drosophila extended lifespan and improved resistance to irradiation. These findings provide evidence supporting the hypothesis that, rather than relying on additional tumour suppressor genes to prevent oncogenesis3,4,5, the bowhead whale maintains genome integrity through enhanced DNA repair. This strategy, which does not eliminate damaged cells but faithfully repairs them, may be contributing to the exceptional longevity and low cancer incidence in the bowhead whale.
Analysis of the longest-lived mammal, the bowhead whale, reveals an improved ability to repair DNA breaks, mediated by high levels of cold-inducible RNA-binding protein.
We developed a single blood-based methylation test that estimates biological aging across 11 physiological systems. This multisystem measure predicts mortality and health outcomes more precisely than existing epigenetic clocks, and reveals distinct aging patterns that could guide personalized gerotherapeutic and geroprotective interventions.