Gestalt Perception and Local-Global Processing in High-Functioning Autism

This study examined gestalt perception in high-functioning autism (HFA) and its relation to tasks indicative of local visual processing. Data on of gestalt perception, visual illusions (VI), hierarchical letters (HL), Block Design (BD) and the Embedded Figures Test (EFT) were collected in adult males with HFA, schizophrenia, depression and normative controls. Individuals with HFA processed gestalt stimuli less in accord with gestalt laws, particularly regarding the principle of similarity. Gestalt processing correlated positively with global processing of the HL. EFT and BD performance correlated negatively with VI susceptibility in HFA. All clinical groups succumbed less to VI than the normative sample. Results suggest decreased gestalt perception in HFA, being associated with a more general local visual processing bias.     

A Case–Control Study of Personality Style and Psychopathology in Parents of Subjects with Autism

To probe the specificity of traits that might be conceptualised as the broader phenotype of autism, parents of subjects with autism from simplex and multiplex families as well as parents of subjects with obsessive–compulsive disorders (OCD), early onset schizophrenia (EOS) and mental retardation (MR) were assessed using the Personality Style and Disorder Inventory and the Symptom Checklist-90-Revised. Autism parents’ scores were increased on several subscales (e.g. reserved/schizoid, depression) compared to parents of subjects with OCD, EOS and normative data, but not in comparison to MR parents. Results provide some support for the specificity of the broader phenotype of autism. The burden of raising severely disabled children could not be ruled out as a factor influencing parts of this phenotype.     

The importance of choline and different serum parameters for the course of the anorexia nervosa

Malnutrition in anorexia nervosa was simulated in an animal starvation study. Female rats aged 11 to 13 weeks received a hypocaloric standard diet or a hypocaloric choline reduced diet. Weight reduction lasted for 12 to 20 weeks and was between 30 % to 40 % of initial weight. Several animals were refed after weight reduction up to 6 to 12 weeks with a standard or a choline enriched diet ad libitum. Serum parameters and membrane fluidity of the CNS were measured after weight reduction or after refeeding. Weight reduction leads to a significant decrease of serum protein, triglycerides (Z = -3.53 resp. -3.42; p < 0.001) and an increase of membrane fluidity in the CNS (Z = -2.83; p < 0.001). Long-term diet with marked weight reduction and following refeeding causes a catabole metabolic situation with significant increase of urea/creatinine-ratio. Choline enriched refeeding after diet results in normalization of serum parameters and membrane fluidity of the CNS. Choline enrichment leads to a significant increase of serum protein (Z = -2.03; p < 0.01). Besides we found a negative correlation between serum protein and urea/creatinine-ratio (r (S) = -0.47; p < 0.001; n = 64). This is possibly caused by a reduced protein catabolism or an increased protein anabolism. Furthermore membrane fluidity in the CNS correlates with serum protein (r (S) = 0.65; p < 0.001; n = 41) and with serum creatinine levels (r (S) = 0.58; p < 0.001; n = 42). We conclude that these serum parameters are potential predictors for cell function in the starved brain and consequently for the course of anorexia nervosa. We furthermore hypothesize that choline enriched nutrition after starvation improves the stabilization of cerebral membranes and the metabolic situation in anorexia nervosa.     

DMBT1 expression distinguishes anorectal from cutaneous melanoma

Aims:  Anorectal melanoma (AM) forms a rare but highly malignant subset of mucosal melanoma with an extremely poor prognosis. Although AMs display histological and immunohistochemical features very similar to cutaneous melanoma (CM), no association exists either with exposure to ultraviolet light or with melanocytic naevi. While AMs are clearly distinguished from CM by displaying few BRAF mutations, they are commonly indistinguishable from CM at the level of gene expression. The aim was to carry out expression analyses of classical immunohistochemical markers and of the protein deleted in malignant brain tumours 1 (DMBT1) in cases of primary anorectal malignant melanoma and CM.
Methods and results:  Expression analyses of classical immunohistochemical markers (S100, HMB45, Melan A and MiTF) and of the protein DMBT1 were carried out in 27 cases of primary anorectal malignant melanoma and 26 cases of CM. All AM cases analysed showed expression of at least three of the classical markers for melanoma. However, immunohistochemistry showed 19 out of 27 AM to be positive for DMBT1, which represented a statistically significant difference ( P  = 0.0009) compared with CM (six out of 26), which more commonly are negative for DMBT1 expression.
Conclusion:  These results identify DMBT1 as a molecular feature that may allow distinction between AM and CM and support the notion that AM represents an entity molecularly distinct from CM.     

Transient intraneuronal Aβ rather than extracellular plaque pathology correlates with neuron loss in the frontal cortex of APP/PS1KI mice

The accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles consisting of hyperphosphorylated tau protein are pathological features of Alzheimer’s disease (AD) commonly modeled in mice using known human familial mutations; however, the loss of neurons also found to occur in AD is rarely observed in such models. The mechanism of neuron degeneration remains unclear but is of great interest as it is very likely an important factor for the onset of adverse memory deficits occurring in individuals with AD. The role of Aβ in the neuronal degeneration is a matter of controversial debates. In the present study we investigated the impact of extracellular plaque Aβ versus intraneuronal Aβ on neuronal cell death. The thalamus and the frontal cortex of the APP/PS1KI mouse model were chosen for stereological quantification representing regions with plaques only (thalamus) or plaques as well as intraneuronal Aβ (frontal cortex). A loss of neurons was found in the frontal cortex at the age of 6 months coinciding with the decrease of intraneuronal immunoreactivity, suggesting that the neurons with early intraneuronal Aβ accumulation were lost. Strikingly, no neuron loss was observed in the thalamus despite the development of abundant plaque pathology with levels comparable to the frontal cortex. This study suggests that plaques have no effect on neuron death whereas accumulation of intraneuronal Aβ may be an early transient pathological event leading to neuron loss in AD. O. Wirths and T. A. Bayer have equally contributed to this work.