Biomedical subjects

Tarja Kauppinen

Publications and source records attributed to Tarja Kauppinen.

3 recordsLinked to original sources

PubMed2006

Human brain tissue microarrays as a platform to investigate diseases of the nervous system.

We constructed tissue microarray (TMA) blocks containing post-mortem human brain tissue from subjects with clinically and neuropathologically verified Alzheimer's disease (AD), corticobasal degeneration (CBD), progressive supranuclear palsy, Lewy body disease, multisystem atrophy (MSA) as well as an age matched control. Fifteen donor blocks were merged into two TMA blocks containing 72, 2-mm punch core samples with representative brain regions generally affected in degenerative disorders. Hyperphosphorylated-gamma, alpha-synuclein and beta-amyloid-related pathologies were estimated. The diseases were easily recognized by evaluating the two TMA sections and the results assessing TMA sections were comparable with the assessment of the whole brain sections. The assessment of TMA sections revealed concomitant multifocal alpha-synuclein pathology in AD, mild tau-involvement in the case of MSA and a slight AD-type pathology in the case of CBD. These findings emphasize the importance of searching for a variety of pathologies in "the whole brain" rather than restricting the examination to a few vulnerable regions. Furthermore, the TMA methodology clearly reduced the number of sections needed for evaluating the whole brain, it increased the amount of research material generated and furthermore no detailed neuroanatomical knowledge was required for assessment of data.

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PubMed2006

Human postmortem brain tissue and 2-mm tissue microarrays.

The authors constructed tissue microarray (TMA) blocks from human postmortem brain including numerous core samples measuring 2 mm in diameter from various anatomic regions. These TMA sections were then processed using various stainings and pretreatment techniques to evaluate their properties. The loss of core samples ranged from 2% to 100% and was significantly influenced by the type of glass slide used; it was lowest (2-8%) with SuperFrost Plus slides. The losses were not significantly altered when applying the most demanding pretreatment procedures or using human brain tissue with a long postmortem delay. A slight influence on the quality and the repeatability of some of the IHC stainings was seen by the postmortem delay, by the brain region, or by the glass slide used. One special feature of the constructed brain TMA block including many anatomic brain regions is that persons who lack skills in neuroanatomy can identify various brain structures simply by following the x-y coordinates. Thus, the applications of this brain TMA block in neurologic research by scientists with different skill bases remain to be determined.

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PubMed2005

Alpha-synuclein pathology does not predict extrapyramidal symptoms or dementia.

Intracytoplasmic aggregation of alpha-synuclein protein as Lewy bodies in the brainstem neurons is diagnostic for Parkinson's disease, whereas if this process also occurs in the cortical neurons, it is considered pathognomonic for dementia with Lewy bodies. However, the link between alpha-synuclein incorporation into inclusions, neuronal dysfunction, and clinical symptoms needs to be clarified. Another important issue of the pathogenetic puzzle is to understand where alpha-synuclein pathology begins and how it progresses in the brain. To study this, we collected all cases from autopsy material (N = 904) that had alpha-synuclein pathology in the dorsal motor nucleus of vagus, substantia nigra, and/or basal forebrain nuclei. In this way, our study has a unique design because the selection of material is entirely based on the presence of alpha-synuclein pathology regardless of clinical phenotype. Retrospective clinical assessment then showed that only 32 (30%) of 106 alpha-synuclein-positive cases were diagnosed with a neurodegenerative disorder. The distribution or load of alpha-synuclein pathology did not permit a dependable postmortem diagnosis of extrapyramidal symptoms or cognitive impairment. Some neurologically unimpaired cases had a reasonable burden of alpha-synuclein pathology in both brainstem and cortical areas, suggesting that alpha-synuclein-positive structures are not definite markers of neuronal dysfunction.

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