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Category: neuroscience

Rethinking the centrality of brain areas in understanding functional organization

For decades, neuroscience textbooks have taught us that the brain is organized into discrete areas — like Broca’s area for language or V1 for early vision, each with a well-defined role. This kind of areal parcellation has shaped how we interpret brain imaging, neural recordings, and even theories of cognition.

But this new article challenges that foundational idea. Instead of treating brain areas as the central units of brain function, the authors argue that brain organization is more complex, multi-layered, and distributed than traditional area-based frameworks suggest.

The authors begin with a simple observation: the ways in which neuroscientists define cortical areas, based on cell structure (cytoarchitecture), connectivity, or response properties — don’t always point to the same boundaries. In other words, different methods of dividing the cortex produce different “maps,” and there’s surprisingly little convergence on a single, definitive set of brain areas.

This inconsistency raises a big question: If areas aren’t consistently defined by structure or connectivity, can we really treat them as the fundamental units of brain function.

Parcellation of the cortex into functionally modular brain areas is foundational to neuroscience. Here, Hayden, Heilbronner and Yoo question the central status of brain areas in neuroscience from the perspectives of neuroanatomy and electrophysiology and propose an alternative approach.

Lipofuscin accumulation in aging and neurodegeneration: a potential “timebomb” overlooked in Alzheimer’s disease

Lipofuscin, a marker of aging, is the accumulation of autofluorescent granules within microglia and postmitotic cells such as neurons. Lipofuscin has traditionally been regarded as an inert byproduct of cellular degradation. However, recent findings suggest that lipofuscin may play a role in modulating age-related neurodegenerative processes, and several questions remain unanswered. For instance, why do lipofuscin granules accumulate preferentially in aged neurons and microglia? What happens to these pigments upon neuronal demise? Particularly in neurodegenerative diseases like Alzheimer’s disease (AD), why does amyloid β (Aβ) deposition usually begin in late adulthood or during aging? Why do lipofuscin and amyloid plaques appear preferentially in grey matter and rarely in white matter? In this review, we argue that lipofuscin should be revisited not as a simple biomarker of aging, but as a potential modulator of neurodegenerative diseases. We synthesize emerging evidence linking lipofuscin to lysosomal dysfunction, oxidative stress, lipid peroxidation and disease onset—mechanisms critically implicated in neurodegeneration. We also explore the potential interactions of lipofuscin with Aβ and their spatial location, and summarize evidence showing that lipofuscin may influence disease progression via feedback loops affecting cellular clearance and inflammation. Finally, we propose future research directions toward better understanding of the mechanisms of lipofuscin accumulation and improved lysosomal waste clearance in aging.

Why consciousness can’t be reduced to code

The familiar fight between “mind as software” and “mind as biology” may be a false choice. This work proposes biological computationalism: the idea that brains compute, but not in the abstract, symbol-shuffling way we usually imagine. Instead, computation is inseparable from the brain’s physical structure, energy constraints, and continuous dynamics. That reframes consciousness as something that emerges from a special kind of computing matter, not from running the right program.

Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque prefrontal cortex

The human brain is a fascinating and complex organ that supports numerous sophisticated behaviors and abilities that are observed in no other animal species. For centuries, scientists have been trying to understand what is so unique about the human brain and how it develops over the human lifespan.

Recent technological and experimental advances have opened new avenues for neuroscience research, which in turn has led to the creation of increasingly detailed descriptions of the brain and its underlying processes. Collectively, these efforts are helping to shed new light on the underpinnings of various neuropsychiatric and neurodevelopmental disorders.

Researchers at Beijing Normal University, the Changping Laboratory and other institutes have recently set out to study both the human and macaque brain, comparing their development over time using various genetic and molecular analysis tools. Their paper, published in Nature Neuroscience, highlights some key differences between the two species, with the human pre-frontal cortex (PFC) developing slower than the macaque PFC.

“Unraveling the cellular and molecular characteristics of human prefrontal cortex (PFC) development is crucial for understanding human cognitive abilities and vulnerability to neurological and neuropsychiatric disorders,” wrote Jiyao Zhang, Mayuqing Li, and their colleagues in their paper. “We created a comparative repository for gene expression, chromatin accessibility and spatial transcriptomics of human and macaque postnatal PFC development at single-cell resolution.”

Human-specific molecular and cellular regulatory programs prolong prefrontal cortical maturation by orchestrating postnatal development of neurons and glia, with implications for cognitive function and susceptibility to neurodevelopmental disorders.

Continue reading “Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque prefrontal cortex” | >

Therapeutic VEGFC treatment provides protection against traumatic-brain-injury-driven tauopathy pathogenesis

How traumatic brain injury (TBI) mechanistically contributes to neurodegenerative disease remains poorly understood. Marco et al. find that therapeutic viral vector-based delivery of VEGFC recuperates meningeal lymphatic drainage deficits post-TBI and protects against severe development of tauopathy, neurodegeneration, and cognitive decline in the PS19 mouse model of tauopathy.

Why the human brain matures slower than its primate relatives

The human brain is a fascinating and complex organ that supports numerous sophisticated behaviors and abilities that are observed in no other animal species. For centuries, scientists have been trying to understand what is so unique about the human brain and how it develops over the human lifespan.

Recent technological and experimental advances have opened new avenues for neuroscience research, which in turn has led to the creation of increasingly detailed descriptions of the brain and its underlying processes. Collectively, these efforts are helping to shed new light on the underpinnings of various neuropsychiatric and neurodevelopmental disorders.

Researchers at Beijing Normal University, the Changping Laboratory and other institutes have recently set out to study both the human and macaque brain, comparing their development over time using various genetic and molecular analysis tools. Their paper, published in Nature Neuroscience, highlights some key differences between the two species, with the human pre-frontal cortex (PFC) developing slower than the macaque PFC.

Scientists found a way to restore brain blood flow in dementia

A new study suggests that dementia may be driven in part by faulty blood flow in the brain. Researchers found that losing a key lipid causes blood vessels to become overactive, disrupting circulation and starving brain tissue. When the missing molecule was restored, normal blood flow returned. This discovery opens the door to new treatments aimed at fixing vascular problems in dementia.

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