History of neuromorphometry

Haug, H

doi:10.1016/0165-0270(86)90110-x

Cited by 100 publications

(72 citation statements)

References 29 publications

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“…Aggregation of modified proteins, disturbance in iron homeostasis, protein and DNA modifications and damage, oxidative stress and impairment of energy production are some of the key mechanisms linking aging to neurodegeneration [2][3][4][5][6]. It was thought for decades that neuron loss plays a key role in the aging process of the CNS [7]. However, more recent research applying advanced quantitative histologic techniques demonstrated that this is not the case (discussed in detail in Section 5).…”

Section: Introductionmentioning

confidence: 88%

“…Until recently it was widely accepted that neuron loss is a general consequence of normal aging, explaining the functional decline of the brain during aging (for review see [7,96,97]). However, with the advent of more accurate procedures for counting neurons, particularly the application of design-based stereologic techniques (for review see [98][99][100]), this view has been modified over the last years.…”

Section: Age-related Neurodegenerationmentioning

confidence: 99%

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Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

et al. 2008

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According to a long-standing hypothesis, aging is mainly caused by accumulation of nuclear (n) DNA damage in differentiated cells such as neurons due to insufficient nDNA repair during lifetime. In line with this hypothesis it was until recently widely accepted that neuron loss is a general consequence of normal aging, explaining some degree of decline in brain function during aging. However, with the advent of more accurate procedures for counting neurons, it is currently widely accepted that there is widespread preservation of neuron numbers in the aging brain, and the changes that do occur are relatively specific to certain brain regions and types of neurons. Whether accumulation of nDNA damage and decline in nDNA repair is a general phenomenon in the aging brain or also shows cell-type specificity is, however, not known. It has not been possible to address this issue with the biochemical and molecular-biological methods available to study nDNA damage and nDNA repair. Rather, it was the introduction of autoradiographic methods to study quantitatively the relative amounts of nDNA damage (measured as nDNA single-strand breaks) and nDNA repair (measured as unscheduled DNA synthesis) on tissue sections that made it possible to address this question in a cell-type-specific manner under physiological conditions. The results of these studies revealed a formerly unknown inverse relationship between age-related accumulation of nDNA damage and age-related impairment in nDNA repair on the one hand, and the age-related, selective, loss of neurons on the other hand. This inverse relation may not only reflect a fundamental process of aging in the central nervous system but also provide the molecular basis for a new approach to understand the selective neuronal vulnerability in neurodegenerative diseases, particularly Alzheimer's disease.

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Section: Introductionmentioning

confidence: 88%

Section: Age-related Neurodegenerationmentioning

confidence: 99%

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

et al. 2008

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“…However, as studies of different brain regions in different species have consistently found that the vascular bed comprises less than 5% of the total brain volume (Haug, 1986;Weis et al, 1996;Lkkegaard et al, 2001), a reduction in the vascular bed could contribute to, but not fully account for, the observed volume reductions.…”

Section: Potential Sources Of the Observed Reductions In Brain Volumementioning

confidence: 99%

The Influence of Chronic Exposure to Antipsychotic Medications on Brain Size before and after Tissue Fixation: A Comparison of Haloperidol and Olanzapine in Macaque Monkeys

Dorph‐Petersen

Pierri

Perel

et al. 2005

Neuropsychopharmacol

373

250

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It is unclear to what degree antipsychotic therapy confounds longitudinal imaging studies and post-mortem studies of subjects with schizophrenia. To investigate this problem, we developed a non-human primate model of chronic antipsychotic exposure. Three groups of six macaque monkeys each were exposed to oral haloperidol, olanzapine or sham for a 17-27 month period. The resulting plasma drug levels were comparable to those seen in subjects with schizophrenia treated with these medications. After the exposure, we observed an 8-11% reduction in mean fresh brain weights as well as left cerebrum fresh weights and volumes in both drug-treated groups compared to sham animals. The differences were observed across all major brain regions (frontal, parietal, temporal, occipital, and cerebellum), but appeared most robust in the frontal and parietal regions. Stereological analysis of the parietal region using Cavalieri's principle revealed similar volume reductions in both gray and white matter. In addition, we assessed the subsequent tissue shrinkage due to standard histological processing and found no evidence of differential shrinkage due to drug exposure. However, we observed a pronounced general shrinkage effect of B20% and a highly significant variation in shrinkage across brain regions. In conclusion, chronic exposure of non-human primates to antipsychotics was associated with reduced brain volume. Antipsychotic medication may confound post-mortem studies and longitudinal imaging studies of subjects with schizophrenia that depend upon volumetric measures.

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“…The problem, of course, is that E(H) is not accessible from independent sections. Apart from the spheres assumption, additional ones relative to truncation (i.e., unobservability or loss of small transects), over and underprojection under slab sectioning, etc., proliferated in the literature from the early 1940's -for a survey in the area of neuroscience see Haug (1986).…”

Section: Particle Numbermentioning

confidence: 99%

Stereology: A Historical Survey

Cruz‐Orive

2017

Image Anal Stereol

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Stereology is the science of geometric sampling, with applications to the statistical analysis of microstructures in biology and materials science. Subsidiary disciplines are image analysis, quantitative microscopy, and radiology. This survey is organized chronologically within a series of topics which cover most aspects of stereology. Each topic is described informally to make it accessible to scientists of different disciplines.

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History of neuromorphometry

Cited by 100 publications

References 29 publications

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

The Influence of Chronic Exposure to Antipsychotic Medications on Brain Size before and after Tissue Fixation: A Comparison of Haloperidol and Olanzapine in Macaque Monkeys

Stereology: A Historical Survey

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