@article{UppalGianatiempoWicinskietal.2014,
  author    = {Uppal, Neha and Gianatiempo, Isabella and Wicinski, Bridget and Schmeidler, James and Heinsen, Helmut and Schmitz, Christoph and Buxbaum, Joseph D. and Hof, Patrick R.},
  title     = {Neuropathology of the posteroinferior occipitotemporal gyrus in children with autism},
  series = {Molecular Autism},
  volume    = {5},
  journal   = {Molecular Autism},
  number    = {17},
  doi       = {10.1186/2040-2392-5-17},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-117275},
  year      = {2014},
  abstract  = {Background: While most neuropathologic studies focus on regions involved in behavioral abnormalities in autism, it is also important to identify whether areas that appear functionally normal are devoid of pathologic alterations. In this study we analyzed the posteroinferior occipitotemporal gyrus, an extrastriate area not considered to be affected in autism. This area borders the fusiform gyrus, which is known to exhibit functional and cellular abnormalities in autism. Findings: No studies have implicated posteroinferior occipitotemporal gyrus dysfunction in autism, leading us to hypothesize that neuropathology would not occur in this area. We indeed observed no significant differences in pyramidal neuron number or size in layers III, V, and VI in seven pairs of autism and controls. Conclusions: These findings are consistent with the hypothesis that neuropathology is unique to areas involved in stereotypies and social and emotional behaviors, and support the specificity of the localization of pathology in the fusiform gyrus.},
  language  = {en}
}
@article{HeinsenStrikLutheretal.1994,
  author    = {Heinsen, Helmut and Strik, M. and Luther, K. and Ulmar, G. and Gangnus, D. and Jungkunz, G. and Eisenmenger, W. and G{\"o}tz, M. and Bauer, M.},
  title     = {Cortical and striatal neurone number in Huntington's disease},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-55217},
  year      = {1994},
  abstract  = {The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five ageand sex-matched control cases. Serial 500-l-lm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36-72 years) was 5.97x 109±320x 106 , the average number of small striatal neurones was 82 X 106± 15.8 X 106• The left striatum (caudatum, putamen, and accumbens) contained a mean of 273 X 106±53 X 106 glial cells (oligodendrocytes, astrocytes and unc1assifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36-75 years) was diminished by about 33 \% to 3.99x109±218x106 nerve cells (P ::;:::: 0.012, MannWhitney V-test). The mean number of small striatal neurones decreased tremendously to 9.72 X 106 ± 3.64 X 106 (-88 \% ). The decrease in total glial cells was less pronounced (193 X 106±26 X 106) but the mean glial index, the numerical ratio of glial cells per neurone, increased from 3.35 to 22.59 in Huntington's disease. Qualitatively, neuronal loss was most pronounced in supragranular layers of primary sensory areas (Brodmann's areae 3,1,2; area 17, area 41). Layer HIc pyramidal cells were preferentially lost in association areas of the temporal, frontal, and parietal lobes, whereas spared layer IV granule cells formed a conspicuous band between layer IH and V in these fields. Methodological issues are discussed in context with previous investigations and similarities and differences of laminar and lobar nerve cellloss in Huntington's disease are compared with nerve cell degent-ration in other neuropsychiatric diseases.},
  subject      = {Medizin},
  language  = {en}
}