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Category: neuroscience – Page 5

Neuropsychiatric symptoms in cognitive decline and Alzheimer’s disease: biomarker discovery using plasma proteomics

Placental toxicology progress!

Commonly used in vitro and in vivo placental models capture key placental functions and toxicity mechanisms, but have significant limitations.

The physiological relevance of placental models varies, with a general hierarchy of simple in vitro complex in vitro/ organ-on-chip in vivo, but species-of origin considerations may alter their relevance to human physiology.

Cellular, rodent, human, and computational modeling systems provide insights into placental transport, physiology, and toxicology linked to maternal–fetal health.

Recent advances in 3D culture and microfluidic technologies offer more physiologically relevant models for studying the placenta.

Mathematical modeling approaches can integrate mechanistic physiological data and exposure assessments to define key toxicokinetic parameters.

Environmental chemical concentrations and omic data obtained from placental tissues can link toxicant influences on placental function to adverse birth outcomes.

Continue reading “Neuropsychiatric symptoms in cognitive decline and Alzheimer’s disease: biomarker discovery using plasma proteomics” | >

New Study Links Altered Cellular States to Brain Structure

Researchers at the Icahn School of Medicine at Mount Sinai have characterized how cellular senescence—a biological process in which aging cells change how they function—is associated with human brain structure in both development and late life. The study, published January 22 in Cell, provides new insight into how molecular signatures of cellular senescence that are present during development and aging mirror those associated with brain volume and cortical organization.

Understanding brain structure is a central challenge in neuroscience. Although brain structure changes throughout life and is linked to both aging and neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases, the underlying molecular processes involved—including cellular senescence—are not defined. Cellular senescence is commonly defined as a state characterized by permanent cell cycle arrest in the absence of cell death, in which cells have altered function. While cellular senescence has been implicated in aging and disease, its role in shaping human brain structure—both during development and aging—has remained unclear.

“This is the first study to directly link senescence-related molecular networks in living human brain tissue to measurable differences in brain structure within the same individuals,” said Noam Beckmann, PhD, Director of Data Sciences and founding member for the Mount Sinai Clinical Intelligence Center, Assistant Professor of Artificial Intelligence and Human Health, and co-senior author of the paper. “By identifying molecular pathways that are engaged in both brain structure development and aging, our work highlights senescence as a fundamental biological feature of brain aging and neurodegenerative disease and helps prioritize targets for future experimental research aimed at protecting brain health.”

Dried blood spot biomarker test for the detection of Alzheimer’s disease

The researchers tested a new method for detecting Alzheimer’s disease using a few drops of blood obtained from the fingertip and then dried on a card. This process was used to find proteins linked to Alzheimer’s disease and other brain changes in the 337 participants.

The study found that levels of p-tau217 in finger-prick samples closely matched results from standard blood tests and were able to identify Alzheimer’s disease-related changes in spinal fluid with an accuracy of 86 per cent. Two other markers, glial fibrillary acidic protein (GFAP) and neurofilament light (NfL), were also successfully measured and showed strong agreement with traditional tests.

While not ready for clinical use, this breakthrough addresses critical barriers in Alzheimer’s research by enabling remote participation in studies, clinical trial recruitment and monitoring, broader population sampling for epidemiological research, and inclusion of underrepresented communities and regions with limited healthcare infrastructure.

The findings suggest that this simple technique could make large-scale studies and remote testing possible, including for people with Down syndrome, who face a higher risk of Alzheimer’s disease and for other underserved populations. ScienceMission sciencenewshighlights.

A groundbreaking international study has demonstrated that Alzheimer’s disease biomarkers can be accurately detected using simple finger-prick blood samples that can be collected at home and mailed to laboratories without refrigeration or prior processing.

The research published in Nature Medicine. It represents the first large-scale validation of this accessible testing approach that removes geographic barriers and opens brain disease research to global populations without requiring specialised healthcare infrastructure.

Continue reading “Dried blood spot biomarker test for the detection of Alzheimer’s disease” | >

Cellular senescence linked to brain structure changes across lifespan

Researchers at the Icahn School of Medicine at Mount Sinai have characterized how cellular senescence—a biological process in which aging cells change how they function—is associated with human brain structure in both development and late life.

The study, published in Cell, provides new insight into how molecular signatures of cellular senescence that are present during development and aging mirror those associated with brain volume and cortical organization.

Understanding brain structure is a central challenge in neuroscience. Although brain structure changes throughout life and is linked to both aging and neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases, the underlying molecular processes involved—including cellular senescence—are not defined.

Abstract: Infiltration of T cell acute lymphoblastic leukemia (ALL) into the meninges worsens prognosis

Ksenia Matlawska-Wasowska & team show T-cell leukemia exploits an inflammatory pathway to invade the brain’s protective layers, revealing a potential target for therapies aimed at preventing disease progression:

The image features GFP⁺ T-ALL leukemic infiltrates within whole-mount murine meningeal tissue. Credit: Wojciech Ornatowski.

1Department of Cell Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA.

2Department of Pediatrics, University of New Mexico, Albuquerque, New Mexico, USA.

3Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama, USA.

A neuron–glia lipid metabolic cycle couples daily sleep to mitochondrial homeostasis

Haynes et al. report a daily, sleep-dependent neuron–glia lipid metabolic cycle. ApoE-dependent lipid transfer from neurons to glia protects neurons from oxidative damage during waking, and lipids are cleared from glia during sleep.

Subcellular depletion of importin β1 impairs presynaptic local translation and spatial memory

Scientists have mapped out an importin-based pathway that enables neurons to maintain synaptic plasticity and spatial memory despite their unusually elongated shape.

Read more in ScienceSignaling.

Axonal localization of importin β1 is required for presynaptic functions that support spatial memory tasks.

Are your memories illusions? New study disentangles the Boltzmann brain paradox

In a recent paper, SFI Professor David Wolpert, SFI Fractal Faculty member Carlo Rovelli, and physicist Jordan Scharnhorst examine a longstanding, paradoxical thought experiment in statistical physics and cosmology known as the “Boltzmann brain” hypothesis—the possibility that our memories, perceptions, and observations could arise from random fluctuations in entropy rather than reflecting the universe’s actual past. The work is published in the journal Entropy.

The paradox arises from a tension at the heart of statistical physics. One of the central pillars of our understanding of the time-asymmetric second law of thermodynamics is Boltzmann’s H theorem, a fundamental concept in statistical mechanics. However, paradoxically, the H theorem is itself symmetric in time.

That time-symmetry implies that it is, formally speaking, far more likely for the structures of our memories, perceptions, and observations to arise from random fluctuations in the universe’s entropy than to represent genuine records of our actual external universe in the past. In other words, statistical physics seems to force us to conclude that our memories might be spurious—elaborate illusions produced by chance that tell us nothing about what we think they do. This is the Boltzmann brain hypothesis.

Brain navigation study reveals function of an unconventional electrical-signaling mode in neurons

Navigating the world is no mean feat, especially when the world pushes back. For instance, airflow hitting a fly on its right side can, after a turn, become a headwind. To stay on course, the fly’s brain must interpret sensations that constantly shift with each turn of its body.

Indeed, transforming changing sensory inputs into a more stable, map-like understanding of the world is intimately connected to an animal’s ability to survive and navigate within its environment. How do flies make it look so easy?

Now, a study published in Cell shows that the fly brain uses a surprisingly economical strategy. Earlier work had demonstrated that flies calculate their direction of travel by combining four neural signals, each encoding motion along a different axis. The new research finds that when it comes to wind direction, the brain doesn’t need four neuronal populations, but only two. This is because each population can handle two opposite directions in the wind system.

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