Despite ample evidence for functional specialization in the brains of humans (Kanwisher, 2010) and nonhuman animals (Tsao et al., 2006), some continue to argue against the idea of stable structure in the brain, emphasizing the distributed, dynamic, and interactive nature of cognitive processes, including language (Pessoa, 2022; Forkel and Hagoort, 2024; Drijvers et al., 2025). Deep engagement with this debate is beyond the scope of this article, but two points are worth clarifying. First, the fact that many areas—sometimes in distant parts of the brain—are engaged by language comprehension does not imply that the “entire brain” supports this function. Although the extended language network spans almost every major component of the brain, within each component, language regions occupy a small fraction of brain tissue. Second, linguistic inputs can unquestionably engage many brain regions beyond those that specifically support language processing: vivid descriptions of faces or scenes can engage category-selective visual areas, a story about a misunderstanding can engage the Theory of Mind network, and a horror story can engage the amygdala (see Casto, et al., 2025b for discussion). However, all these brain regions can also be engaged by nonlinguistic inputs. The ability of a brain region to be engaged by language does not make it a “language region” any more than its ability to be engaged by visual inputs makes it a “visual region.” Furthermore, the fact that the language network needs to interact with other brain areas does not undermine its functional distinctness from those areas and its special role in language processing. As long as different components within the language network interact more strongly with one another than with other networks—for which ample evidence exists (Blank et al., 2014; Braga et al., 2020; Du et al., 2024, 2025; Shain and Fedorenko, 2025)—the language network and other cognitive networks can be treated as meaningfully distinct objects of study (Simon, 1962).
For completeness and ease of comparison with past studies, we explored the possibility of using standard anatomical atlases to constrain individual fROIs (rather than the parcels derived from a group-level representation of brain activity; Fedorenko et al., 2010; Julian et al., 2012). Examining individual activation maps (or maps derived from functional connectivity patterns: Braga et al., 2020; Du et al., 2024, 2025; Shain and Fedorenko, 2025) against standardized brain parcellations reveals two issues. First, individual topographies often do not align with the boundaries of the atlas areas: a contiguous functional region may get broken up by a boundary or—for finer-grained atlases—may get assigned to different atlas areas across individuals because of interindividual topographic variability (see Fig. S5B for examples). For studies focusing on a particular functional network, we therefore recommend functional parcels over anatomical/multimodal atlases.
One of the hallmarks of Alzheimer’s disease is the accumulation of a peptide in the brain known as amyloid beta. A new study published in Nature Communications on July 22 has uncovered the atomic structure of the peptide in its harmful form.
Amyloid beta is a naturally occurring peptide that exists in healthy brains. But in Alzheimer’s disease, these peptides clump together abnormally and form large plaques. Scientists have known about the association between these plaques and Alzheimer’s disease for over a century, but whether this buildup is actually damaging the brain or simply a byproduct of the disease has been hotly debated.
There is also an intermediate state of amyloid beta that exists between the healthy peptides and the large plaques. Emerging evidence suggests that it is these intermediates—so-called “oligomeric” amyloid beta—that drive damage to the brain, but their structure has remained unknown. Now, a team of researchers at Yale School of Medicine has characterized this intermediate form for the first time.
Results from a small clinical trial suggest it may be possible to reduce the risk of dementia by eating during fewer hours of the day. The pilot study, which involved a weight-loss program for older women with overweight or obesity, showed modest cognitive improvements among those who limited their daily eating window instead of just reducing their calorie intake.
“Losing weight alone will ward off some of the aging-related cognitive decline, and these data suggest that there may be additional benefits if you stop eating four hours before going to sleep and reduce food intake to 8–9 hours per day, compared with the usual eating window of 12 hours per day,” said Sue Shapses, Ph.D., RD, DFASN, professor at Rutgers University and Rutgers-RWJ Medical Center and the study’s principal investigator.
Shapses’ group will present the findings at NUTRITION 2026, the flagship annual meeting of the American Society for Nutrition, held July 25–28 in National Harbor, Maryland, just outside Washington, D.C.
A study of 4,818 middle-aged and older Chinese adults found that higher light BioAge was associated with greater risks of cognitive impairment, episodic memory decline, and reduced mental intactness. The simple measure, based on age, creatinine, glucose, and CRP, added modest predictive information but requires further validation before clinical use.
Seeing feels immediate; we open our eyes and the world seems to appear as a continuous stream. But some visual illusions show that events occurring later can change how we perceive what happened earlier, suggesting that the brain may collect and combine information for a short time before producing the experience that reaches awareness.
This effect is known as “postdiction.” Here’s an example: Two colored dots appear briefly in different places, but people see only a single moving dot that changes color along the way. This means that the second dot must influence how the first is perceived, a typical example of postdiction.
The frontal cortex (FC) has been implicated in many of the cognitive and executive control functions required for goal-directed behavior (Komura et al., 2001; Bruni et al., 2015; Duan et al., 2021; Friedman and Robbins, 2021), including decision-making (Coley et al., 2021; Liu et al., 2021), response inhibition (Schiller et al., 2014; Li et al., 2020), working memory (O’Reilly and Frank, 2006; Miller et al., 2018; Wilhelm et al., 2023), attentional control (Zikopoulos and Barbas, 2007; Gregorlou et al., 2014), and adaptive modulation of sensory filters (Banerjee et al., 2020). In the auditory system, cortical neurons can rapidly adapt their receptive field tuning and spectrotemporal selectivity reflecting changing stimulus context and task conditions (Fritz et al., 2003, 2005, 2007; David et al., 2012; Yin et al., 2014; Elgueda et al., 2019). This task-related receptive field plasticity may be shaped by changing functional connectivity between FC and auditory cortex (Fritz et al., 2010; Sheikhattar et al., 2018; Yin et al., 2020). This adaptive capacity is critical since context can transform the behavioral meaning of incoming stimuli and even cause the same sound to mean two opposite things in different circumstances.
In this study, we explored the role of the FC in this adaptive decision-making process by employing the same sounds to signify diametrically opposite meanings depending on task context and reward valence. In one behavioral paradigm, upon hearing a Target sound, animals initiated licking to obtain a water reward (positive reward; P-paradigm). In the other paradigm, animals learned to stop licking for water when presented with the same Target stimulus in order to avoid a mild shock (negative reward; N-paradigm). In an earlier study (David et al., 2012), we found that such different task reward structures and stimulus-action contingencies induced two strikingly distinct forms of receptive field plasticity in primary auditory cortex (A1). In light of the strong top-down projections from the FC to auditory cortex (AC) influencing dynamic sensory filters (Caras and Sanes, 2017; Bimbard et al., 2018; Schneider et al., 2018; Winkowski et al., 2018; Mittelstadt and Kanold, 2023; Macedo-Lima et al., 2024), we wondered whether the differential receptive plasticity was driven by distinct FC representations of the two opposite behavioral paradigms.
Therefore, we trained two groups of ferrets on two opposite auditory categorical Go-NoGo paradigms, requiring each group to discriminate noncompact sound categories (Yin et al., 2016, 2020). Task stimuli varied along two acoustic feature dimensions: spectral frequency (TN-task) or temporal modulation rate (amplitude-modulated white noise, AM-task). As indicated above, in the P-paradigm group, ferrets learned to lick for water reward when Target stimuli were presented and refrained from licking to Reference stimuli. In contrast, the group that learned the N-paradigm performed the opposite behavior and refrained from licking for water when Target stimuli were presented but could lick freely to Reference sounds (Fig. 1 A).
Biomedical engineers at Duke University have developed an injectable biomaterial that helps transform the cavity left behind after a stroke caused by a blood clot into an environment more supportive of repair. By recruiting the body’s own immune cells, the treatment promoted the growth of new blood vessels, supported neural remodeling and improved motor performance in mice. The work appears in Cell Biomaterials.
Every year, millions of people experience strokes caused by blood clots, called ischemic strokes. Immediate treatments, including clot-dissolving drugs and mechanical removal of the clot, can restore blood flow and preserve threatened brain tissue. But these treatments cannot replace tissue that has already been lost.
Large strokes can result in substantial tissue loss and leave behind a cavity at the site of the injury. After the clot is removed, recovery relies largely on rehabilitation, which helps surviving brain circuits adapt but does not directly repair the damaged area.
For decades, neuroscientists have searched the brain for the biological basis of consciousness, assuming our thoughts, emotions, and subjective experiences emerge from networks of neurons.
But what if that assumption is incomplete?
That’s the provocative question explored by neuroscientist Christof Koch of the Allen Institute in Seattle.
For most of human history, scientists believed that once a cell became a skin cell, a neuron, or a heart cell, that identity was permanent. Then a group of researchers discovered something extraordinary: cells could be reset. My guest today was there when that discovery happened.
Dr. Koji Tanabe, Ph.D. is Founder and CEO of I Peace (https://ipeace.com/en/), one of the world’s leading companies advancing induced pluripotent stem cell — or iPSC — technology from the research laboratory into scalable clinical manufacturing.
Dr. Tanabe occupies a truly unique place in modern biomedical history. He earned his Ph.D. in the laboratory of Nobel Laureate Dr. Shinya Yamanaka at Kyoto University and was the second author on the landmark scientific paper that first demonstrated the successful creation of human induced pluripotent stem cells — a discovery that fundamentally changed regenerative medicine and ultimately earned Dr. Yamanaka the 2012 Nobel Prize.
After helping establish one of the most important technologies in modern biology, Dr. Tanabe continued his work at Stanford University in the laboratory of Dr. Marius Wernig, a pioneer of direct cellular reprogramming, where he investigated how mature blood cells can be directly converted into neurons and explored the molecular mechanisms that govern cellular identity.
In 2015, Dr. Tanabe founded I Peace with an ambitious vision: to make clinical-grade iPS cells accessible at industrial scale. Today, the company has developed automated GMP manufacturing platforms capable of producing personalized and clinical-grade iPS cells for researchers, pharmaceutical companies, and regenerative medicine programs around the world.
On the episode we’ll explore how far the field has come since those first groundbreaking experiments nearly two decades ago, where regenerative medicine stands today, the growing role of iPS cells in drug discovery and transplantation, the excitement surrounding in vivo reprogramming and partial cellular rejuvenation, and what may ultimately become possible when every individual has access to their own personalized stem cell bank.