PubMed HealthSearch

PubMed · 7754292

Neurocognitive networks and selectively distributed processing.

Abstract

The association cortex of the human brain can be divided into unimodal and transmodal components. Unimodal (modality-specific) cortical areas are subdivided into upstream regions specialized for encoding unitary features of experience and downstream regions which are specialized for encoding composite features. Modality-specific features lead to multimodal knowledge through the mediation of transmodal areas in the brain. These transmodal areas include cortical regions that are conventionally designated as heteromodal, paralimbic and limbic cortex. Contrary to earlier formulations, it is no longer thought that these transmodal areas contain a convergent residue of knowledge. Instead, it appears that the role of these transmodal areas is to contain a road map for the multifocal binding and calling up of distributed information in multiple modalities. Knowledge can thus be encoded in a flexible distributed rather than rigid convergent form. Observations on patients with focal neurological lesions indicate that transmodal areas act like neural hubs (or gateways) for accessing critical domains of knowledge rather than as dedicated centers for specific cognitive functions. In the processes related to memory, a limbic structure such as the hippocampus does not act as a bank for specific memories but as a critical node for accessing distributed information related to recently acquired experience. Damage to a sufficient volume of the limbic system interferes with the coherence of recall and storage even though the constituent fragments of the corresponding experiences may remain stored quite well in other parts of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Mesulam. Neurocognitive networks and selectively distributed processing.. https://pubmed.ncbi.nlm.nih.gov/7754292/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex

Pigment variant of neuronal ceroid-lipofuscinosis.

A 6-year-old girl had progressive ataxia, and visual disturbances resulting in blindness. She died in her sleep at age 22 years. She shared with her sister and paternal relatives bilateral pes cavus deformities and impaired deep-tendon reflexes which suggested Charcot-Marie-Tooth disease. Her sister, who also had both polyneuropathy and a progressive central nervous system (CNS) disease, did not have pigmentary retinopathy. At autopsy, the patient was found to have neuronal ceroid-lipofuscinosis (NCL) marked by intraneuronal accumulation of autofluorescent granular lipopigments in ballooned perikarya and conspicuous extraneuronal pigmentation of subcortical grey matter, but without axonal spheroids. These findings indicate a pigment variant of NCL and represent one of very few patients recorded. The ultrastructure of the intraneuronal pigments was uniformly granular, while that of the extraneuronal pigments found within processes of the neuropil and glial perikarya was more variegated. In addition to those patients with the pigment variant of NCL, described earlier by Jakob and Kolkmann [1973: Acta Neuropathol (Berl) 26:225-236], and Jervis and Pullarkat [1978: Neurology 28:500-503], our patient shared clinical symptoms with those described in a family afflicted with polyneuropathy and NCL by Wisniewski et al. [1987: J Child Neurol 2:33-41]. Currently, it is unclear whether they have similar atypical forms of juvenile NCL (JNCL). We conclude that the spectrum of pigment variants in lysosomal diseases is heterogeneous: only few and recently described patients have had NCL, while others most likely had other forms of lipidosis.

Cerebral Cortex