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Cerebral cortex astroglia and the brain of a genius: a propos of A. Einstein's.

ABSTRACT: The glial fibrillary acidic protein immunoreactive astroglial layout of the cerebral cortex from Albert Einstein and other four age-matched human cases lacking any known neurological disease was analyzed using quantification of geometrical features mathematically defined. Several parameters (parallelism, relative depth, tortuosity) describing the primate-specific interlaminar glial processes did not show individually distinctive characteristics in any of the samples analyzed. However, A. Einstein's astrocytic processes showed larger sizes and higher numbers of interlaminar terminal masses, reaching sizes of 15 microm in diameter. These bulbous endings are of unknown significance and they have been described occurring in Alzheimer's disease. These observations are placed in the context of the general discussion regarding the proposal--by other authors--that structural, postmortem characteristics of the aged brain of Albert Einstein may serve as markers of his cognitive performance, a proposal to which the authors of this paper do not subscribe, and argue against.

SUBMITTER: Colombo JA

PROVIDER: S-EPMC2935295 | biostudies-literature | 2006 Sep

REPOSITORIES: biostudies-literature

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Cerebral cortex astroglia and the brain of a genius: a propos of A. Einstein's.

Colombo Jorge A JA Reisin Hernán D HD Miguel-Hidalgo José J JJ Rajkowska Grazyna G

Brain research reviews 20060503 2

The glial fibrillary acidic protein immunoreactive astroglial layout of the cerebral cortex from Albert Einstein and other four age-matched human cases lacking any known neurological disease was analyzed using quantification of geometrical features mathematically defined. Several parameters (parallelism, relative depth, tortuosity) describing the primate-specific interlaminar glial processes did not show individually distinctive characteristics in any of the samples analyzed. However, A. Einstei ...[more]

PMID: 16675021

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Project description:Astroglia from the postnatal cerebral cortex can be reprogrammed in vitro to generate neurons following forced expression of neurogenic transcription factors, thus opening new avenues towards a potential use of endogenous astroglia for brain repair. However, in previous attempts astroglia-derived neurons failed to establish functional synapses, a severe limitation towards functional neurogenesis. It remained therefore also unknown whether neurons derived from reprogrammed astroglia could be directed towards distinct neuronal subtype identities by selective expression of distinct neurogenic fate determinants. Here we show that strong and persistent expression of neurogenic fate determinants driven by silencing-resistant retroviral vectors instructs astroglia from the postnatal cortex in vitro to mature into fully functional, synapse-forming neurons. Importantly, the neurotransmitter fate choice of astroglia-derived neurons can be controlled by selective expression of distinct neurogenic transcription factors: forced expression of the dorsal telencephalic fate determinant neurogenin-2 (Neurog2) directs cortical astroglia to generate synapse-forming glutamatergic neurons; in contrast, the ventral telencephalic fate determinant Dlx2 induces a GABAergic identity, although the overall efficiency of Dlx2-mediated neuronal reprogramming is much lower compared to Neurog2, suggesting that cortical astroglia possess a higher competence to respond to the dorsal telencephalic fate determinant. Interestingly, however, reprogramming of astroglia towards the generation of GABAergic neurons was greatly facilitated when the astroglial cells were first expanded as neurosphere cells prior to transduction with Dlx2. Importantly, this approach of expansion under neurosphere conditions and subsequent reprogramming with distinct neurogenic transcription factors can also be extended to reactive astroglia isolated from the adult injured cerebral cortex, allowing for the selective generation of glutamatergic or GABAergic neurons. These data provide evidence that cortical astroglia can undergo a conversion across cell lineages by forced expression of a single neurogenic transcription factor, stably generating fully differentiated neurons. Moreover, neuronal reprogramming of astroglia is not restricted to postnatal stages but can also be achieved from terminally differentiated astroglia of the adult cerebral cortex following injury-induced reactivation.

Project description:BackgroundTraumatic brain injury (TBI) initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent.ResultsAmong the upregulated genes 1 day post injury, were transcription factors and genes involved in metabolism, e.g. STAT-3, C/EBP-delta and cytochrome p450. At 4 days post injury we observed increased gene expression of inflammatory factors, proteases and their inhibitors, like cathepsins, alpha-2-macroglobulin and C1q. Notably, genes with biological function clustered to immune response were significantly upregulated 4 days after injury, which was not found following 1 day. Osteopontin and one of its receptors, CD-44, were both upregulated showing a local mRNA- and immunoreactivity pattern in and around the injury site. Fewer genes had decreased expression both 1 and 4 days post injury and included genes implicated in transport, metabolism, signalling, and extra cellular matrix formation, e.g. vitronectin, neuroserpin and angiotensinogen.ConclusionThe different patterns of gene expression, with little overlap in genes, 1 and 4 days post injury showed time dependence in genomic responses to trauma. An early induction of factors involved in transcription could lead to the later inflammatory response with strongly upregulated CD-44 and osteopontin expression. An increased knowledge of genes regulating the pathological mechanisms in trauma will help to find future treatment targets. Since trauma is a risk factor for development of neurodegenerative disease, this knowledge may also reduce late negative effects.

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Cerebral cortex astroglia and the brain of a genius: a propos of A. Einstein's.

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Cerebral cortex astroglia and the brain of a genius: a propos of A. Einstein's.

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