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Category: neuroscience

A bonobo’s imaginary tea party suggests apes can play pretend

The findings add to a growing body of work suggesting that ape minds can imagine scenarios beyond the “here-and-now,” a skill once thought to be unique to humans. Human children begin playing pretend as early as 12 months old and master the ability to build imaginary worlds by age 3. Many high-level thinking tasks are possible only because we can imagine things that aren’t really there.

The study centered on Kanzi, a remarkable bonobo who could communicate using word-linked symbols called lexigrams. Amalia Bastos, a comparative psychologist at the University of St Andrews in Scotland, first met him in 2023. “We were starstruck by Kanzi,” she says.

During their first meeting, the bonobo used his lexigram-studded board to ask Bastos and a colleague to chase each other. Bastos noticed that even though they only pretended to play, Kanzi still enjoyed watching them. This kick-started a series of make-believe tests that Bastos and Christopher Krupenye, a psychologist at Johns Hopkins University, designed for Kanzi.

In the first of these tests, Kanzi sat at a table with two glasses. An experimenter pretended to pour a glass of “juice” — Kanzi’s tipple of choice — into both cups from a see-through empty jug. The experimenter then poured the nonexistent contents of one cup back into the jug, before asking Kanzi which cup still held the “juice.” Kanzi guessed correctly 68 percent of the time, significantly above chance, the researchers report.

The guesses, Bastos says, may not have been definitive evidence of Kanzi’s internal imagination. “Kanzi is an old bonobo. Maybe his vision isn’t very good. Maybe he thinks that there’s real juice in these things,” she says.

The researchers retested Kanzi to see if he could identify real from fake juice. They presented him with two cups: one containing orange juice and an empty one that they filled with pretend juice. When asked which cup he wanted, Kanzi picked the real juice nearly 80 percent of the time, suggesting he had little issue identifying his reward. A third test that mimicked the first, but with pretend grapes rather than juice, again suggested Kanzi understood where pretend food was located.

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Eyes may be a window into early Alzheimer’s detection

The eyes—specifically, the outer area of the retina—may provide a window into early detection of Alzheimer’s disease (AD) long before irreversible brain damage has occurred, according to new research from Houston Methodist. This discovery could dramatically change how the disease is diagnosed, monitored and treated.

“Retinal Müller glia alterations and their impact on ocular glymphatic clearance in an Alzheimer’s disease mouse model,” is online and will appear in an upcoming edition of the Journal of Alzheimer’s Disease. Led by Stephen Wong, Ph.D., the John S. Dunn Presidential Distinguished Chair in Biomedical Engineering at Houston Methodist and director of T. T. & W. F. Chao Center for BRAIN, the study reveals how the peripheral retina (versus the central retina) could be a window into early diagnosis of AD.

“The eyes are indeed a window into the brain, but our study reveals that we have been looking at the wrong part of the window,” Wong said. “While most clinical eye exams focus on the central retina, the most critical early indicators of AD appear to be hidden at the periphery of the eye. By identifying these retinal changes that occur before the brain’s ‘plumbing’ system fails, doctors may eventually be able to use routine eye exams to catch and treat the disease years before memory loss begins.”

Alzheimer’s ‘Clock’ Uses Blood Test to Forecast Symptom Onset

Researchers developed a “clock” model that based on a single blood test can estimate Alzheimer’s symptom onset in cognitively unimpaired adults.

The model predicted onset age with a roughly 3-year median margin of error.

— Findings could streamline enrollment for Alzheimer’s clinical trials.

Radiologic Biomarkers in Multiple Sclerosis: Improving Detection and Diagnosis

MRI is central to modern MultipleSclerosis diagnosis.

A review article by Drs. Elfasi and Fagundo highlights radiologic lbiomarkers in the 2024 McDonald criteria—including the central vein sign, paramagnetic rim lesions, cortical lesions, and optic nerve imaging.

https://ow.ly/cZrC50Yj69O National Multiple Sclerosis Society ACTRIMS American Academy of Neurology (AAN) Radiological Society of North America (RSNA) University of South Florida.

Imaging biomarkers, including cortical lesions, the central vein sign, and paramagnetic rim lesions, allow for more timely and accurate diagnosis of multiple sclerosis.

Scientists Believe Quantum Computers AreAbout to Cross a Major Line

We began this inquiry by looking at the mismatch between our computers and our brains. We realized that we were trying to run biological software on the wrong hardware. That era is ending. As we refine these quantum processors, we are finally building a mirror that is accurate enough to reflect the true nature of the mind. We are not just building faster computers. We are building a vessel that can hold the physics of thought.

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Timestamps:
0:00 Quantum Computers.
1:18 The Scale Problem.
4:40 The Thermodynamic Wall.
8:11 Quantum Mechanics in Wetware.
13:58 The \

Scientists Grew Mini Brains, Then Trained Them to Solve an Engineering Problem

A few blobs of lab-grown brain tissue have demonstrated a striking proof of concept: living neural circuits can be nudged toward solving a classic control problem through carefully structured feedback.

In a closed-loop system that delivered electrical feedback based on performance, cortical organoids could steadily improve their control of a classic engineering benchmark: balancing an unstable virtual pole.

The improvement is far from a functioning hybrid biocomputer. But as a proof of concept, it shows that neural tissue in a dish can be adaptively tuned through structured feedback – a result that could help researchers probe how neurological disease alters the brain’s capacity for plasticity.

Frontiers: Psoriasis is a complex, chronic relapsing and inflammatory skin disorder with a prevalence of approximately 2% in the general population worldwide

Psoriasis can be triggered by infections, physical injury and certain drugs. The most common type of psoriasis is psoriasis vulgaris, which primarily features dry, well-demarcated, raised red lesions with adherent silvery scales on the skin and joints. Over the past few decades, scientific research has helped us reveal that innate and adaptive immune cells contribute to the chronic inflammatory pathological process of psoriasis. In particular, dysfunctional helper T cells (Th1, Th17, Th22, and Treg cells) are indispensable factors in psoriasis development. When stimulated by certain triggers, antigen-presenting cells (APCs) can release pro-inflammatory factors (IL-23, IFN-α and IL-12), which further activate naive T cells and polarize them into distinct helper T cell subsets that produce numerous cytokines, such as TNF, IFN-γ, IL-17 and IL-22, which act on keratinocytes to amplify psoriatic inflammation. In this review, we describe the function of helper T cells in psoriasis and summarize currently targeted anti-psoriatic therapies.

Psoriasis is a complex, chronic relapsing and inflammatory skin disorder with an overall prevalence of 2% in the general population worldwide (1). The most common type of psoriasis is psoriasis vulgaris, which primarily manifests as dry, well-demarcated, raised red lesions with adherent silvery scales on the skin and joints and accounts for nearly 90% of all psoriasis cases. Psoriasis is also associated with multiple comorbidities, such as arthritis, obesity, diabetes mellitus, depression, hypertension, cardiovascular disease, and reduced quality of life (2).

Although the exact mechanism that triggers psoriasis remains unclear, it is currently accepted that psoriasis is induced or exacerbated by either nonspecific triggers, such as infections [such as Streptococcus ], physical injury [such as scratching and tattoos ], drugs [such as β blockers, lithium and antimalarials (5, 6)] or some specific autoantigens [such as cathelicidin LL-37, melanocytic ADAMTSL5, lipid antigen PLA2G4D and keratin 17 ]. Pathologically, psoriasis is characterized by epidermal acanthosis (thickening of the viable layers), hyperkeratosis (thickened cornified layer), and parakeratosis (cell nuclei present in the cornified layer).

Astrocytes enable amygdala neural representations supporting memory

A thorough study exploring how astrocytes affect fear conditioning and fear extinction in the basolateral amygdala of mice. Subpopulations of astrocytes were found to interact with neurons in such a way as to help encode representations of fear. [ https://www.nature.com/articles/s41586-025-10068-0](https://www.nature.com/articles/s41586-025-10068-0)

Gq G-protein-coupled receptor (GPCR) signalling increases astrocyte Ca2+ activity through IP3-mediated release of intracellular Ca2+ stores42,43 and hM3Dq actuation causes a Ca2+ surge preceded by prolonged quiescence, possibly due to intracellular Ca2+ depletion24,44,45. Replicating these effects in the BLA, we expressed hM3Dq in BLA astrocytes and used in vivo cyto-GCaMP6f photometry and observed that clozapine–N-oxide (CNO) injection markedly increased Ca2+ activity within around 10 min but, thereafter, decreased and remained low for at least 2 h (Fig. 2c and Extended Data Figs. 6a–e and 8e, f). A lower hM3Dq virus concentration or lower CNO dose had modest or negligible effects on Ca2+ activity and behaviour (Extended Data Fig. 6h–p). On the basis of these data, we posited that BLA astrocyte Ca2+ dynamics would be constrained by hM3Dq actuation at timepoints relevant to behavioural testing. Consistent with this supposition, hM3Dq-actuation essentially abolished Ca2+ responses to a potent stimulus (footshock) given 30 min after CNO injection (Extended Data Fig. 6f, g).

We leveraged these effects of hM3Dq actuation to test how constraining astrocyte Ca2+ dynamics affected memory acquisition, retrieval, consolidation and extinction by injecting separate groups of animals with 3 mg per kg CNO either before or immediately after F-Con, or before fear retrieval/extinction training. We found that CNO given before extinction training reduced CS-related freezing during E-Ext—consistent with impaired memory retrieval—in hM3Dq-expressing mice compared with viral controls (Fig. 2d, e). In vivo fibre photometry confirmed that this behavioural effect was accompanied by loss of CS-related astrocyte Ca2+ responses (Fig. 2f and Extended Data Fig. 7a–c). In contrast to these memory-retrieval-impairing effects, CNO had no behavioural effect when injected before or after F-Con26,27 and did not alter uncued freezing, shock-induced flinching or various measures of anxiety-like behaviour (Extended Data Fig. 7d–i). Behavioural effects were also absent when CNO was injected in mice not expressing hM3Dq or when vehicle was injected in hM3Dq-expressing animals, excluding potential non-specific CNO and hM3Dq-virus effects, respectively (Extended Data Fig. 7j–n).

We next compared these effects with those of another DREADD, hM4Di, that produces effects on cortical, striatal and (as we show here; Fig. 2g–i) BLA astrocyte Ca2+ activity that mirror those of hM3Dq, that is, increase Ca2+ transients24,46,47. Accordingly, we found that hM4Di actuation produced effects on memory retrieval that were opposite to hM3Dq: pre-Ext CNO injection produced increases in CS-related freezing and astrocyte Ca2+ responses during E-Ext in hM4Di-expressing mice compared with viral controls (Fig. 2j–l and Extended Data Fig. 8a–f). Pre-Ext hM4Di actuation also increased freezing during (CNO-free) E-Ret, indicative of a deficit in extinction memory formation, and attenuated CS-related Ca2+ activity during this test stage. This latter effect is notable given that hM3Dq actuation produced a similar extinction deficit and blunted the CS-related Ca2+ response on E-Ret (Fig. 2e and Extended Data Fig. 7b), despite the two manipulations having opposite effects on fear retrieval and neither affecting extinction memory when CNO was given before E-Ret (Extended Data Fig. 8g, h). This convergence of extinction-impairing effects suggests that extinction is sensitive to perturbations—whether increases or decreases—in astrocyte Ca2+ activity and, by extension, implies an important role for BLA astrocytes in the plastic adaptations underlying extinction memory formation.

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