Hematopoietic aging extends far beyond the confines of the bone marrow, functioning as a central regulator of systemic decline through its influence on inflammation, immune dysregulation, and inter-organ communication. Moreover, reciprocal signaling from peripheral organs, such as the brain and gut, further shapes hematopoietic aging, highlighting the bidirectional nature of these interactions (Figure 3).
The potential use of psychedelics in the treatment of various mental health conditions has made these drugs a hot area of scientific research, as well as growing public interest. A variant of ketamine called esketamine is already FDA approved and utilized for treatment-resistant depression, and the FDA has designated formulations of psilocybin and MDMA for the treatment of depression and PTSD, respectively, as “breakthrough therapies,” a process designed to expedite their development and review. NIDA is actively funding research on these compounds—NIDA and the National Institute on Mental Health are the largest funders of psychedelic research at NIH—as they represent a potential paradigm shift in the way we address substance use disorders too. Yet there is much we still do not know about these drugs, the way they work, and how to administer them, and there is danger of the hype getting out ahead of the science.
The promise of psychedelic compounds likely centers on their ability to promote rapid neural rewiring.1 Recent preclinical studies have suggested that the “neuroplastogen” properties of psilocybin, for example, may have to do with its ability to bind to 5HT2A (serotonin) receptors inside neurons, something that serotonin itself cannot do.2 That rewiring may explain these compounds’ relatively long-lasting effects, even with just one or a few administrations. Some trials have found effects lasting weeks3, but smaller studies (and anecdotes) are suggestive of much longer durations. What is needed is sound scientific research including clinical trials that can substantiate therapeutic efficacy, duration, and safety in large numbers of participants.
As part of a research study, psychedelics are administered by clinicians within highly controlled settings. This is important not only for safety reasons but because contextual factors and expectations play a crucial role in their effectiveness.4 Whether a patient has a positive or negative experience depends to a significant extent upon their mindset going into the experience and whether the setting is one in which they feel secure. This raises an important question—the extent (if any) to which the clinician’s time and attention and/or therapeutic approach play a role in psychedelics’ therapeutic efficacy—where much more research is needed. The extent to which psychotherapy is necessary in conjunction with psychedelics and which methods work best is an open question.
Despite its diminutive size, the organ packs almost 500 feet of wiring and 54.5 million synapses into the size of a grain of sand — an astonishing feat of computational neurology research that allows scientists to better understand how signals travel throughout the brain.
And thanks to significant advances of some of the world’s most capable supercomputers, researchers at the Jülich Research Centre in Germany are now aiming their sights at a far more ambitious goal: a simulation at the scale of the entire human brain.
Previous attempts, dating back a decade, like the Human Brain Project, fell largely flat, despite considerable government funding. But as New Scientist reports, the Jülich researchers think they can push things forward. The idea is to bring together several models of smaller regions of the brain with a supercomputer to run simulations of billions of firing neurons.
A landmark international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age.
The findings — based on more than 10,000 MRI scans and over 13,000 memory assessments from 3,700 cognitively healthy adults across 13 studies — show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer’s-associated genes like APOE ε4. This suggests that brain aging is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology.
Published in Nature Communications, the study, “Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change,” found that structural brain change associated with memory decline is widespread, rather than confined to a single region. While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships. This suggests that cognitive decline in aging reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions. The pattern across regions formed a gradient, with the hippocampus at the high end and progressively smaller but still meaningful effects across large portions of the brain.
https://www.nature.com/articles/s41467-025-66354-y
Genetic risk for Alzheimer’s and widespread brain shrinkage linked to greater memory loss — even in otherwise healthy adults.
Paternal genetic risk is a robust predictor of offspring psychiatric disorders, with additional “indirect genetic effects” observed for internalizing and substance use conditions in adoptive and stepfather relationships. Rearing effects were most pronounced for substance use disorders.
Question In an adoption study of major psychiatric illness, what results would be obtained if offspring risk were predicted not from the phenotype of the parents but from their genetic risk?
Findings In this cohort study, paternal genetic risk was associated with offspring risk of illness for all disorders in genetically related father-offspring pairs. In an indirect pathway, genetic risk in adoptive and stepfathers predicted risk in their offspring for internalizing and substance use disorders but not for schizophrenia or bipolar disorder.
Meaning Indirect genetic effects from the father may have an impact on offspring risk of internalizing and substance use disorders.
Researchers at the Children’s Cancer Institute and UNSW Sydney have tested a new way of treating childhood brain cancer by combining two medicines in lab studies. They found using the two treatments together may work better than using either on its own. The research is published in the journal Science Translational Medicine.
In the new study, Children’s Cancer Institute and UNSW Sydney researchers lab-tested a combined therapy approach on a group of difficult-to-treat brain tumors: diffuse midline gliomas (DMG). This group includes diffuse intrinsic pontine glioma (DIPG), a rare but fatal childhood brain cancer. Children diagnosed with DIPG usually survive for about 12 months.
UNSW Conjoint Professor David Ziegler and UNSW Conjoint Associate Professor Maria Tsoli led the study. They have been working for many years to find better treatments for DIPG.