Do autism spectrum disorders differ from each other and from non-spectrum disorders on emotion recognition tests?

 We tested whether dimensional measures of empathic ability, theory of mind, and intelligence would differentiate autism spectrum disorders from each other and from non-spectrum disorders. Tests were administered to children with a diagnosis of Autistic Disorder (AutD; n = 20), Asperger's Disorder (AspD; n = 28), Attention Deficit/Hyperactivity Disorder (Inattentive Type) (ADHD; n = 35), Mental Retardation (Mild) (MR; n = 34), Anxiety Disorder (AnxD; n = 14), or No Psychological Disorder (NPD; n = 36). Results showed that empathic ability discriminated among groups on the autism spectrum (AutD < AspD < NPD). Because empathic ability is not independent of intelligence (AutD < AspD < NPD on intelligence; MR < ADHD < NPD on empathic ability), both dimensions are necessary to discriminate autism spectrum from non-spectrum disorders. When intelligence is covaried, empathic ability discriminated AutD, but not AspD, from other disorders (AutD < MR < ADHD <  NPD = AnxD = AspD). Accepted: 11 October 2000     

Decreased β-Cell Function is Associated with Cardiovascular Autonomic Neuropathy in Chinese Patients Newly Diagnosed with Type 2 Diabetes

The influence of β-cell function on cardiovascular autonomic neuropathy (CAN), an important diabetes-related complication, is still unclear. In this study, we aimed to investigate the association between residual β-cell function and CAN in patients newly diagnosed with type 2 diabetes. We enrolled 90 newly-diagnosed type 2 diabetic patients and 37 participants with normal glucose tolerance as controls. The patients were divided into a CAN+ group (diabetic patients with CAN, n = 20) and a CAN− group (diabetic patients without CAN, n = 70) according to the standard Ewing battery of tests. Fasting and postprandial plasma glucose, insulin, and C-peptide were measured. Homeostasis model assessment-beta cells (HOMA-B) and HOMA-insulin resistance (IR) were calculated. The prevalence of CAN in this population was 22.2%. Compared with the CAN− group, the CAN+ group had significantly lower fasting plasma insulin (6.60 ± 4.39 vs 10.45 ± 7.82 μ/L, P = 0.029), fasting C-peptide (0.51 ± 0.20 vs 0.82 ± 0.51 nmol/L, P = 0.004), and HOMA-B (21.44 ± 17.06 vs 44.17 ± 38.49, P = 0.002). Fasting C-peptide was correlated with the Valsalva ratio (r = 0.24, P = 0.043) and the 30:15 test (r = 0.26, P = 0.023). Further analysis showed that fasting C-peptide (OR: 0.041, 95% CI 0.003–0.501, P = 0.012) and HOMA-B (OR: 0.965, 95% CI 0.934–0.996, P = 0.028) were independently associated with cardiovascular autonomic nerve function in this population. The patients with fasting C-peptide values < 0.67 nmol/L were more likely to have CAN than those with C-peptide levels ≥0.67 nmol/L (OR: 6.00, 95% CI 1.815–19.830, P = 0.003). A high prevalence of CAN was found in patients with newly-diagnosed type 2 diabetes. Decreased β-cell function was closely associated with CAN in this population.     

Amyloid β-protein (Aβ)-containing astrocytes are located preferentially near N-terminal-truncated Aβ deposits in the human entorhinal cortex

The deposition of the amyloid β-protein (Aβ) is a pathological hallmark of Alzheimer’s disease (AD). Aβ is a peptide consisting of 39–43 amino acids and is derived by β- and γ-secretase cleavage from the Aβ protein precursor (AβPP). An N-terminal-truncated form of Aβ can occur following α- and γ-secretase cleavage of AβPP. Fleecy amyloid is a recently identified distinct type of Aβ deposits occurring in the internal layers (pri-α, pri-β and pri-γ) of the human entorhinal cortex. Fleecy amyloid consists exclusively of N-terminal-truncated Aβ and is a transient form of Aβ deposits, which disappears in late-stage β-amyloidosis. In this study, the entorhinal cortex of 15 cases with AD-related pathology was used to examine astrocytes in the vicinity of N-terminal-truncated Aβ in fleecy amyloid of the layers pri-α, pri-β, and pri-γ in comparison to astrocytes in the vicinity of full-length Aβ in layers pre-β and pre-γ. Immunohistochemistry was performed with antibodies directed against AβPP, Aβ₄₀, Aβ₄₂, Aβ_17–24, Aβ_1–17 and Aβ_8–17 as well as by double-labeling with antibodies directed against Aβ_17–24, Aβ₄₂, and glial fibrillary acid protein (GFAP). A large number of GFAP-positive astrocytes containing N-terminal-truncated Aβ fragments appeared in the vicinity of N-terminal-truncated Aβ, whereas Aβ-containing astrocytes were rarely seen in the vicinity of full-length Aβ. These results suggest that N-terminal-truncated Aβ peptide may be cleared preferentially from the extracellular space by astrocytic uptake and processing. Such an astroglial uptake of N-terminal-truncated Aβ may account for the transient nature of fleecy amyloid and point to the use of N-terminal truncation of Aβ in potential therapeutic strategies aimed at preventing the brain from amassing full-length Aβ deposits. Received: 20 August 1999 / Revised, accepted: 14 March 2000     

Social interaction modifies neural response to gaze shifts

Monitoring gaze shifts is important for social interactions.The direction of gaze can reveal intentions and help to predictfuture actions. Here we examined whether behavioural and neuralresponses to gaze shifts were modulated by the social contextof the gaze shift in two linked experiments. Two faces werepresented, one gazing directly at the subject (the ‘social’face) and one with averted gaze (the ’unsocial’face). One face then made a gaze shift that was either towardsa visible target (’correct’) or towards anotherlocation in space (’incorrect’). Both behaviouraland neural responses to gaze shifts were modulated by the socialcontext and the goal directedness of the gaze shift. Reactiontimes were significantly faster in response to ’correct’and ‘social’ compared with ’incorrect’and ’unsocial’ gaze shifts, respectively. Usingfunctional magnetic resonance imaging, we found significantlygreater activation in the parieto-frontal attentional network,and in some parts of the posterior superior temporal sulcus,in response to ‘incorrect’ and ’unsocial’compared with ’incorrect’ and ‘social’gaze shifts, respectively. Conversely, we found greater activationin the medial prefrontal cortex and precuneus in response to’correct’ and ‘social’ compared with’incorrect’ and ’unsocial’ gaze shifts.This activity may reflect the experience of joint attentionassociated with these gaze shifts.     

The Ca2+/calmodulin-dependent protein kinase II-associated protein complex isolated from chicken retina

Activated microglia represent a major source of inflammatory factors in Alzheimer’s disease and a possible source of cytotoxic factors. β-Amyloid (Aβ) peptide, the predominant component in amyloid plaques, has been shown to activate microglia and stimulate their production of inflammatory factors. The present study was performed to analyze the responses of microglia to different forms of Aβ, with regard to release of the proinflammatory cytokines interleukin-1α (IL-1α), IL-1β, tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ), as well as the IL-1 receptor antagonist (IL-1ra). Primary cultures of microglia from rat neonatal cerebral cortex were incubated with freshly dissolved Aβ_1–40 or Aβ_1–42, Aβ_1–40 fibrils, Aβ_1–40 βamy balls, or vehicle. Aβ_1–40 fibrils did not significantly stimulate any of these cytokines. Freshly dissolved Aβ_1–40 resulted in a marked increase in the release of IL-1β, and freshly dissolved Aβ_1–42 significantly stimulated both IL-1α and IFN-γ secretion. The Aβ_1–40 βamy balls stimulated the secretion of IL-1α and IL-1β. Incubation with Aβ peptides did not affect the secretion of IL-1ra, IL-6, or TNF-α. In the case of IL-1β, the response is correlated with the presence of Aβ peptide as monomers and oligomers.     

Ultrastructural localization of α-, β- and γ-sarcoglycan and their mutual relation, and their relation to dystrophin, β-dystroglycan and β-spectrin in normal skeletal myofiber

Ultrastructural localization of α-, β- and γ-sarcoglycan and their mutual relation, and their relation to dystrophin, β-dystroglycan and β-spectrin were investigated in normal skeletal myofibers. Single-immunogold labeling electron microscopy showed that the signals of rabbit and sheep polyclonal antibodies against the synthetic peptide of the cytoplasmic domain of α-, β or γ-sarcoglycan were present along the inside surface of muscle plasma membrane and at the sarcoplasmic side of plasma membrane invaginations and vesicular structures in subsarcolemmal areas. These localizations were similar to that of dystrophin, β-dystroglycan and β-spectrin. Double-immunogold labeling disclosed the close association of α-, β- and γ-sarcoglycan each other and α-, β-, γ-sarcoglycan with dystrophin or β-dystroglycan, and this was confirmed by statistical analysis. Monoclonal antibody against the extracellular domain of α-sarcoglycan was used with above-mentioned polyclonal anti-β- and -γ-sarcoglycan antibodies for triple-immunogold labeling, in which signals of α-sarcoglycan localized at the outer surface of muscle plasmalemma and those of β- and γ-sarcoglycans were present at the inside surface of plasma membrane. The triple immunolabeling showed an occasional closely associated presence of the three signals for α-, β- and γ-sarcoglycans, and a more frequent association for two signals out of α-, β- and γ-sarcoglycans. This study demonstrated that α-, β- and γ-sarcoglycan are closely located to one another and to dystrophin and β-dystroglycan at the muscle plasma membrane. Received: 22 June 1998 / Revised: 7 September 1998 / Accepted: 14 September 1998     

Mikrochirurgie lumbaler Bandscheibenvorf?lle üerlegene Ergebnisse der Mikrochirurgie im Vergleich zu Standard- und perkutanen Verfahren (Literaturübersicht) üerlegene Ergebnisse der Mikrochirurgie im Vergleich zu Standard- und perkutanen Verfahren (Literaturübersicht)

Der Wert verschiedener Operationstechniken lumbaler Bandscheibenvorf?lle wurde anhand einer Literaturmetaanalyse untersucht.Standarddiskektomie ohne Mikroskop (5.080 Operationen/9 Serien) und Mikrodiskektomie (5.354/23) wurden einzeln analysiert und miteinander verglichen (2.494/10); Chemo- (2.729/16), Lasernukleolyse (644/3), 3 Arten perkutaner Nukleotomie (3.357/18) wurden einzeln analysiert und untereinander (942/5) mit der Mikrochirurgie (561/5) oder der Standarddiskektomie (1.020/6) verglichen. Outcome-Kategorien (Macnab) waren: I “sehr gut”, II “gut”, III “besser als pr?operativ”,“Schmerzmittelbedarf”, IV “praktisch gleich”, V “schlechter”; I/II “deutlich gebessert”, III “zum Teil gebessert”, IV/V “nicht gebessert”; I–III(“erfolgreich” bzw. IV/V “erfolglos”.     

Allosteric Modulator Desformylflustrabromine Relieves the Inhibition of α2β2 and α4β2 Nicotinic Acetylcholine Receptors by β-Amyloid<Subscript>1–42</Subscript> Peptide

Nicotinic acetylcholine receptors (nAChRs) are pentameric transmembrane proteins that belong to the cys-loop ligand-gated ion channel family. These receptors are widely expressed in the brain and implicated in the pathophysiology of many neurological conditions, including Alzheimer’s disease (AD), where typical symptoms include the loss of cognitive function and dementia. The presence of extracellular neuritic plaques composed of β amyloid (Aβ_1–42) peptide is a characteristic feature of AD. Desformylflustrabromine (dFBr) is a positive allosteric modulator (PAM) for α4β2 nAChRs since it increases peak ACh responses without inducing a response on its own. Previously, the effect of dFBr on the α2β2 nAChR subtype was not known. The action of dFBr was tested on α2β2 receptors expressed in Xenopus oocytes. It was found that dFBr is also a PAM for the α2β2 receptor. Next we tested whether dFBr had any effect on the previously known block of both the α4β2 and α2β2 receptors by Aβ_1–42. We found that the functional blockade of ACh-induced currents in oocytes expressing α4β2 and α2β2 receptors by Aβ_1–42 was prevented by dFBr. We conclude that dFBr is a positive allosteric modulator for both α4β2 and α2β2 subtypes of nAChRs and that it also relieves the blockade of these receptors by Aβ_1–42. This study demonstrates that PAMs for the non-α7 nAChRs have the potential to develop into clinically applicable drugs for AD and other disorders.     

Circulating B7-H3(CD276) Elevations in Cerebrospinal Fluid and Plasma of Children with Bacterial Meningitis

The objective of this study was to analyze the clinical significance of cerebrospinal fluid (CSF) and plasma concentrations of B7-H3, tumor necrosis factor-alpha (TNF-α), gamma interferon (IFN-γ), and interleukin-17 (IL-17) in bacterial and aseptic meningitis in children. The participants were six children with bacterial meningitis, 16 with aseptic meningitis, and 12 control subjects. All participants were between 2 months and 12 years of age on admission. Cytokines determination was performed by enzyme-linked immunosorbent assay technique. CSF and plasma-circulating B7-H3 were significantly higher in the bacterial meningitis group as compared with the aseptic group (p = 0.001) and the control group (p = 0.000 and p = 0.001 respectively). However, CSF and plasma-circulating B7-H3 in aseptic meningitis were not significantly higher than control group (p = 0.071 and p = 0.72 respectively).CSF and plasma-circulating TNF-α were significantly higher in the bacterial meningitis group as compared with the aseptic group (p = 0.004 and p < 0.0001 respectively) and control group (p = 0.004 and p < 0.0001 respectively). Similarly, we did not observe significant elevated TNF-α levels in CSF and plasma in aseptic group compared with control group (p = 0.03 and p = 0.12 respectively). IFN-γ levels in CSF and plasma were undetectable in control group, and we did not find statistical significances in both of CSF and plasma between the elevated IFN-γ level in bacterial meningitis group and aseptic meningitis group(p = 0.055 and p = 0.095 respectively) CSF and plasma levels of IL-17 were undetectable in all subjects. There were correlations between B7-H3 and TNF-α, IFN-γ (r = 0.875, p = 0.000; r = −0.693, p = 0.000, respectively) in CSF in meningitis subjects. In plasma, levels of B7-H3 in bacterial meningitis on admission correlated positively with TNF-α (r = 0.968, p = 0.002), and white blood cell counts (r = 0.973, p = 0.001). Detectable CSF levels of B7-H3, TNF-α, and IFN-γ on admission were not associated significantly with any of CSF characteristics. Additionally, CSF and plasma levels of B7-H3 decreased remarkably after treatment. Altogether, our data indicated that circulating B7-H3 and TNF-α levels in the CSF and plasma were useful markers for distinguishing bacterial from aseptic meningitis, and Circulating B7-H3 was demonstrated to be useful in evaluating the intensity of the infectious inflammatory process in the central nervous system in children. An erratum to this article can be found at     

Implementing Evidence-Based Practices for Youth in an HMO: The Roles of External Ratings and Market Share

A qualitative study of child clinicians in a non-profit HMO examined implementation of evidence-based practices (EBPs) for anxiety and oppositional defiant disorders using interviews and focus groups with 33 clinicians (97% of participants), and ethnography of emails and meetings. Analysis showed statistical measures of access and service—key elements of rating organizations’ “report cards”— were central in creating “pressure” making transition to EBPs difficult. EBPs were secondary to access and service targets. “Research” and “statistics” were perceived as unrealistic, “literature” as lacking authority. Rating organizations should include outcome and fidelity metrics to align market share pressures with children’s health.     

Psychosis and transformation: A phenomenological inquiry

Conventional views towards psychosis typically portray psychosis as an illness of the brain with a generally poor prognosis, even if treated with antipsychotics. However, there is a growing body of literature which presents an alternative view of psychosis, whereby people are not only able to recover from psychosis, but can also experience transformative and/or spiritual growth through psychosis. To learn more about the transformative potential of psychotic experiences, a phenomenological approach was used to research the experiences of six people who self-identified as having benefited from psychosis in a spiritual and/or transformative manner. Keys themes emerging from interviews with these six individuals included in the pre-psychosis phase “childhood foreshadowing” and “negative childhood events,” and in the psychosis phase, “sudden psychosis,” “psychic/intuitiveness and unusual visual experiences,” “comprised day-to-day functioning,” “experiences of dying,” and “communication with god.” Four themes made up the transformation of psychosis phase including “detachment and mindfulness,” “accepting the dissolution of time into now,” “embracing a spiritual pathway,”“ and ”re-alignment of career path.“ Overall, the results suggest that at least for some individuals, the experience of psychosis can be an important catalyst for spiritual and personally transformative growth.     

Limited correlation between systemic biomarkers and neurocognitive performance before and during HIV treatment

The AIDS Clinical Trials Group (ACTG) study A5303 investigated the associations between neuropsychological performance (NP) and inflammatory biomarkers in HIV-infected participants. Fifteen NP tests were administered at baseline and week 48 to 233 ART naïve participants randomized to maraviroc- or tenofovir-containing ART. Neurocognition correlated modestly with markers of lymphocyte activation and inflammation pre-ART (percent CD38+/HLA-DR+(CD4+) (r = − 0.22, p = 0.02) and percent CD38+/HLA-DR+(CD8+) (r = − 0.25, p = 0.02)), and with some monocyte subsets during ART (r = 0.25, p = 0.02). Higher interleukin-6 and percent CD38+/HLA-DR+(CD8+) were independently associated with worse severity of HIV-associated neurocognitive disorders (HAND) (p = 0.04 and 0.01, respectively). More studies to identify HAND biomarkers are needed.     

Alzheimer disease macrophages shuttle amyloid-beta from neurons to vessels, contributing to amyloid angiopathy

Neuronal accumulation of oligomeric amyloid-β (Αβ) is considered the proximal cause of neuronal demise in Alzheimer disease (AD) patients. Blood-borne macrophages might reduce Aβ stress to neurons by immigration into the brain and phagocytosis of Αβ. We tested migration and export across a blood-brain barrier model, and phagocytosis and clearance of Αβ by AD and normal subjects’ macrophages. Both AD and normal macrophages were inhibited in Αβ export across the blood-brain barrier due to adherence of Aβ-engorged macrophages to the endothelial layer. In comparison to normal subjects’ macrophages, AD macrophages ingested and cleared less Αβ, and underwent apoptosis upon exposure to soluble, protofibrillar, or fibrillar Αβ. Confocal microscopy of stained AD brain sections revealed oligomeric Aβ in neurons and apoptotic macrophages, which surrounded and infiltrated congophilic microvessels, and fibrillar Aβ in plaques and microvessel walls. After incubation with AD brain sections, normal subjects’ monocytes intruded into neurons and uploaded oligomeric Aβ. In conclusion, in patients with AD, macrophages appear to shuttle Aβ from neurons to vessels where their apoptosis may release fibrillar Aβ, contributing to cerebral amyloid angiopathy. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. J. Zaghi and B. Goldenson contributed equally.     

Characterization of Aβ11-40/42 peptide deposition in Alzheimer’s disease and young Down’s syndrome brains: implication of N-terminally truncated Aβ species in the pathogenesis of Alzheimer’s disease

Senile plaques (SPs), one of two defining lesions of Alzheimer’s disease (AD), are composed of a mixture of full-length Aβ1-40/42, and N- or C-terminally truncated Aβ peptides, including Aβ11-40/42. Sequential proteolysis of amyloid precursor protein (APP) by β- and γ-secretases produces Aβ1-40/42, but β-site APP-cleaving enzyme 1 (BACE1), the major β-secretase, also generates Aβ11-40/42, and BACE1 overexpression in cultured cells results primarily in secretion of Aβ11-40/42. The ratio of Aβ11-40/42 to Aβ1-40/42 depends on the ratio of BACE1 to APP, and Aβ11-40/42 can be generated from both full-length APP and its carboxy-terminal fragment (C99). Here, we investigated the role of Aβ11-40/42 in the pathogenesis of AD and Down’s syndrome (DS) brains. We demonstrated significant amount of Aβ11-42 in DS brains by Western blots. While pyroAβ11-42-modified Aβ species existed predominantly in mature SP cores in AD brain sections, both unmodified free Aβ11-40 and pyro-modified Aβ11-40 are detected in vascular amyloid deposits by immunohistochemistry. Using novel ELISAs for quantifying free Aβ11-40/42 and pyroAβ11-40/42, we showed that insoluble Aβ11-42 predominated in extracts of AD and DS brains. This is the first systematic study of Aβ11-40/42 in neurodegenerative Aβ amyloidosis implicating Aβ11-40/42 in SP formation of AD and DS brains. The detection of Aβ11-42 in young DS brain suggests an early role for this N-terminally truncated Aβ peptide in the pathogenesis of SPs in AD and DS.     

Medical Histories of Control Subjects Influence the Biomarker Potential of Plasma Aβ in Alzheimer’s Disease: a Meta-analysis

Whether blood amyloid-β (Aβ) could be a peripheral biomarker of Alzheimer’s disease (AD) remains in dispute. In the present study, we conducted a meta-analysis with 19 citations searched from Embase, PubMed, and the Cochrane Library database. Weighted mean difference (WMD) with 95% confidence intervals (CIs) was used to estimate the effect size. We firstly analyzed the plasma Aβ40, Aβ42, and Aβ42/Aβ40 ratio in AD and control group subjects. However, only a lower level of plasma Aβ42 was figured out in AD group subjects with weak statistical significance (WMD 1.82; 95% CI 0.59, 3.06; P = 0.004; I2 = 84%). We considered that the medical histories of control subjects could influence the biomarker ability of plasma Aβ. Therefore, subgroup analyses were then carried out based on a new recruiting criterion for control subjects, defining as no afflictions of any Aβ-related diseases. Surprisingly, AD group subjects showed a significant decrease in plasma Aβ42/Aβ40 ratio with low heterogeneity among studies (WMD 0.02; 95% CI 0.02, 0.02; P < 0.00001; I2 = 0%). Moreover, not only the Aβ42/Aβ40 ratio but also Aβ42 and Aβ40 were indifferent between AD and pseudo-control subjects which might be afflicted with Aβ-related diseases. This meta-analysis demonstrated that medical histories of control subjects were interference factors impeding plasma Aβ to be a biomarker of AD.     

Frau F. sorgt zunehmend für sich selbst

Aus ihren theoretischen Konzeptionen und ihrer grundsätzlichen Haltung ergibt sich für die Integrative Gestalttherapie (IG) die Notwendigkeit, verschiedene diagnostische Perspektiven einzunehmen und zu integrieren. Die Vielfalt der Perspektiven ermöglicht es, der Absolutsetzung einer Perspektive entgegenzuwirken, und fördert die Einsicht, dass kein Diagnosesystem – sei es noch so ausgefeilt – die Wirklichkeit eines Menschen erfassen kann. Menschen mit defizitären oder traumatisierenden Entwicklungsbedingungen (besonders in den ersten Lebensjahren) haben eingeschränkte Möglichkeiten zur Entwicklung ihrer strukturellen Fähigkeiten. Selbstregulierung, kreative Anpassung und Selbstaktualisierung in verschiedenen Lebensbereichen sind dadurch geprägt und die Lebensqualität oft deutlich beeinträchtigt. Die Integration von Strukturdiagnostik in der IG-Diagnostik durch die Einbeziehung von OPD‑2 ermöglicht eine differenziertere Einschätzung und Orientierung über Ressourcen und Defizite von Patient*innen. Die mehrperspektivische diagnostische Herangehensweise – unter Einbeziehung der in der Leitlinie des Gesundheitsministeriums vorgesehenen Diagnoseschritte bei besonderer Berücksichtigung des unmittelbaren Beziehungsgeschehens und der Entwicklungsgeschichte – ermöglicht eine differenzierte Sicht auf die ganze Person im therapeutischen Kontext und im Lebensumfeld. Das unterstützt eine auf die Person und ihre Verarbeitungsfähigkeit abgestimmte therapeutische Vorgehensweise, Schwerpunktsetzung und Beziehungsgestaltung, welche im therapeutischen Prozess dialogisch den jeweiligen Möglichkeiten und Bedürfnissen der Person angepasst werden kann. Menschen auf gutem Strukturniveau mit konflikthafter Thematik profitieren von anderen therapeutischen Angeboten als Personen mit strukturellen Defiziten. Im folgenden Beitrag soll die Verschränkung von Grundkonzepten der Integrativen Gestalttherapie und zentraler Punkte psychodynamischer Diagnostik (nach OPD-2) skizziert werden. Anhand einer kurzen Fallvignette werden aus diagnostischer und therapeutischer Perspektive und unter besonderer Berücksichtigung struktureller Einschätzung wesentliche therapeutische Vorgehensweisen dargestellt.     

Apolipoprotein E4 promotes the early deposition of Aβ42 and then Aβ40 in the elderly

The apolipoprotein Eɛ4 allele (ApoEɛ4) is associated with a selective increase in deposition of the 40-amino acid form of the β-amyloid peptide (Aβ40) in end-stage Alzheimer’s disease. To determine how apoE genotype affects the early events in β-amyloid pathogenesis, we analyzed the medial temporal lobes of 244 elderly persons who were not clinically demented using antibodies selective for the C termini of Aβ40 and Aβ42. We found that: (1) the number of both Aβ42- and Aβ40-positive senile plaques increase with age; (2) Aβ42 appears at younger ages, and in more amyloid deposits, than does Aβ40 in all ApoE groups; (3) when compared at similar ages, older persons with ApoEɛ4 are more likely to have Aβ42- and Aβ40-immunoreactive deposits than are persons without ApoEɛ4; (4) Aβ40-containing plaques arise at least a decade later than do Aβ42 plaques, and are seldom found in the medial temporal lobe of older persons lacking ApoEɛ4; and (5) in the absence of overt Alzheimer’s disease, cerebral amyloid angiopathy is rare in the elderly, but in our sample was significantly augmented in ApoEɛ4 homozygotes. We conclude that ApoEɛ4 hastens the onset of Aβ42 deposition in the senescent brain, which in turn fosters the earlier evolution of fibrillar, Aβ40-positive plaques, thereby increasing the risk of Alzheimer’s disease. Received: 18 June 1999 / Revised: 8 October 1999 / Accepted: 12 October 1999     

Psychometric Evaluation of the Life Orientation Test—Revised in Treated Opiate Dependent Individuals

We examined internal consistency and test-retest reliability of a measure of dispositional optimism, the Life Orientation Test — Revised, in 121 opiate-dependent patients seeking methadone treatment. Internal consistency was adequate at baseline (α = .69) and follow-up (α = .72). Low socioeconomic status and being on disability were significantly associated with reduced internal consistency; ethnic and educational differences approached significance. Test-retest reliability was good (ICC = .72), varying across gender, race, ethnicity, education, employment and income (ICC Range = .24 –.85). Criterion validity was strong; the LOT-R was significantly negatively correlated with hopelessness (r = -.65, p < .001) and depression (r = -.60, p < .001). Findings support the use of this measure of optimism and pessimism to assess positive cognitive and emotional attributes and improve treatment strategies for opiate-dependent individuals. Future research should address the measurement and significance of optimism in minority, low socioeconomic status and poorly-educated individuals.     

Der familiäre Hintergrund „suchtbelastete Familie“ und dessen Auswirkung auf Mentalisierungsprozesse fremduntergebrachter Kinder

Studien über Bindung weisen auf Schwierigkeiten drogenabhängiger Eltern hinsichtlich ihrer Reaktion auf die emotionalen Signale der Kinder und die daraus abzuleitenden Verhaltensweisen hin. Dies lässt auf eine reduzierte Mentalisierungsfähigkeit schließen. Mentalisieren bedeutet die grundlegende menschliche Fähigkeit, Verhalten in Bezug auf Gedanken und Gefühle zu verstehen. Um diese Fähigkeit bei fremduntergebrachten Kinder (6–12 Jahre) aus suchtbelasteten Familien und deren aktuellen Bezugspersonen zu untersuchen, wurde eine auf dem Konzept der Mentalisierung basierende Gruppenintervention entwickelt, die das Wissen über Drogenabhängigkeit erweitern und soziale und affektive Fähigkeiten verbessern soll. Erhebungsinstrumente: Skala des Reflective Functioning (RF-Score) für das Adult Attachment Interview und für das Child Attachment Interview, Inventar der Sozialkompetenzen (ISK), Coloured Progressive Matrices (CPM), Child Behavior Checklist (CBCL/6-18R), „Patte-Noire“-Test, Einstellungen zum Drogenkonsum (EBDD Bewertungsinstrument). An Hand zweier Fallbeispiele aus dieser laufenden Pilotstudie, werden der diagnostische Prozess sowie beobachtbare und messbare Veränderungen über den Untersuchungszeitraum von mehr als 12 Monaten exemplarisch dargestellt und diskutiert.