Retinal vascular dysfunction relates to cognitive impairment in Alzheimer's disease

Cerebral vascular dysregulation has been increasingly implicated as a risk factor in the development of Alzheimer disease (AD)1; however, because of the difficulties associated with assessing and visualizing the cerebral vasculature directly, the ability to detect such dysregulation, noninvasively, is currently limited.2 Consequently, one concept that is being increasingly explored is the possibility of using the eye as a "window to the brain"; this approach has reasonable scientific validity as the retinal and brain vessels share a large number of embryological, anatomic, and functional similarities.2 Indeed, previous research has demonstrated a correlation between cognition and the geometry of the retinal vessels in elderly people.3 The aim of this pilot study, therefore, was to explore whether microvascular functional anomalies are evident at the retinal level in mild AD patients and to determine whether these anomalies relate to the degree of concurrent cognitive deficit..

The temporal binding deficit hypothesis of autism

Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.

Localizing the deficit in a case of jargonaphasia

We report the case of a neologistic jargonaphasic and ask whether her target-related and abstruse neologisms are the result of a single deficit, which affects some items more severely than others, or two deficits: one to lexical access and the other to phonological encoding. We analyse both correct/incorrect performance and errors and apply both traditional and formal methods (maximum-likelihood estimation and model selection). All evidence points to a single deficit at the level of phonological encoding. Further characteristics are used to constrain the locus still further. V.S. does not show the type of length effect expected of a memory component, nor the pattern of errors associated with an articulatory deficit. We conclude that her neologistic errors can result from a single deficit at a level of phonological encoding that immediately follows lexical access where segments are represented in terms of their features. We do not conclude, however, that this is the only possible locus that will produce phonological errors in aphasia, or, indeed, jargonaphasia.

Attention deficits in dyslexia:Evidence for an automatisation deficit?

Both attentional difficulties and rapid processing deficits have recently been linked with dyslexia. We report two studies comparing the performance of dyslexic and control teenagers on attentional tasks. The two studies were based on two different conceptions of attention. Study 1 employed a design that allowed three key components of attention - focusing, switching, and sustaining - to be investigated separately. One hypothesis under investigation was that rapid processing problems - in particular impaired ability to switch attention rapidly - might be associated with dyslexia. However, although dyslexic participants were significantly less accurate than their controls in a condition where they had to switch attention between two target types, the nature of the deficit suggested that the problem was not in switching attention per se. Thus, in Study 2, we explored an alternative interpretation of the Study 1 results in terms of the classic capacity-limited models of "central" attention. We contrasted two hypotheses: (1) that dyslexic teenagers have reduced cognitive resources versus (2) that they suffer from a general impairment in the ability to automatise basic skills. To investigate the automaticity of the shape recognition component of the task a similar attention paradigm to that used in Study 1 was employed, but using degraded, as well as intact, stimuli. It was found that stimulus degradation led to relatively less impairment for dyslexic than for matched control groups. The results support the hypothesis that dyslexic people suffer from a general impairment in the ability to automatise skills - in this case the skill of automatic shape recognition.

Predicting dyslexia using prereading skills:the role of sensorimotor and cognitive abilities

Background: It is well established that phonological awareness, print knowledge and rapid naming predict later reading difficulties. However, additional auditory, visual and motor difficulties have also been observed in dyslexic children. It is examined to what extent these difficulties can be used to predict later literacy difficulties. Method: An unselected sample of 267 children at school entry completed a wide battery of tasks associated with dyslexia. Their reading was tested 2, 3 and 4 years later and poor readers were identified (n = 42). Logistic regression and multiple case study approaches were used to examine the predictive validity of different tasks. Results: As expected, print knowledge, verbal short-term memory, phonological awareness and rapid naming were good predictors of later poor reading. Deficits in visual search and in auditory processing were also present in a large minority of the poor readers. Almost all poor readers showed deficits in at least one area at school entry, but there was no single deficit that characterised the majority of poor readers. Conclusions: Results are in line with Pennington’s (2006) multiple deficits view of dyslexia. They indicate that the causes of poor reading outcome are multiple, interacting and probabilistic, rather than deterministic. Keywords: Dyslexia; educational attainment; longitudinal studies; prediction; phonological processing.

Cognitive-behavioural phenotype in a group of girls from 1.2 to 12 years old with the Incontinentia Pigmenti syndrome:recommendations for clinical management

Incontinentia Pigmenti (IP, OMIM#308300) is a rare X-linked genomic disorder (about 1,400 cases) that affects the neuroectodermal tissue and Central Nervous System (CNS). The objective of this study was to describe the cognitive-behavioural profile in children in order to plan a clinical intervention to improve their quality of life. A total of 14 girls (age range: from 1 year and 2 months to 12 years and 10 months) with IP and the IKBKG/NEMO gene deletion were submitted to a cognitive assessment including intelligence scales, language and visuo-spatial competence tests, learning ability tests, and a behavioural assessment. Five girls had severe to mild intellectual deficiencies and the remaining nine had a normal neurodevelopment. Four girls were of school age and two of these showed no intellectual disability, but had specific disabilities in calculation and arithmetic reasoning. This is the first description of the cognitive-behavioural profile in relation to developmental age. We stress the importance of an early assessment of learning abilities in individuals with IP without intellectual deficiencies to prevent the onset of any such deficit.