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At least 1,531 records · Page 85Linked to original sources
PubMed2004

Developmental origins of the age-related decline in cortical cholinergic function and associated cognitive abilities.

Ontogenetic abnormalities in the regulation of the cortical cholinergic input system are hypothesized to mediate early-life cognitive limitations (ECL) that later escalate, based on reciprocal interactions between a dysregulated cholinergic system and age-related neuronal and vascular processes, to mild cognitive impairment (MCI) and, subsequently, for a majority of subjects, senile dementia. This process is speculated to begin with the disruption of trophic factor support of the basal forebrain ascending cholinergic system early in life, leading to dysregulation of cortical cholinergic transmission during the initial decades of life and associated limitations in cognitive capacities. Results from neurochemical and behavioral experiments support the possibility that aging reveals the vulnerability of an abnormally regulated cortical cholinergic input system. The decline of the cholinergic system is further accelerated as a result of interactions with amyloid precursor protein metabolism and processing, and with cerebral microvascular abnormalities. The determination of the developmental variables that render the cortical cholinergic input system vulnerable to age-related processes represents an important step toward the understanding of the role of this neuronal system in the age-related decline in cognitive functions.

Acetylcholine↗
PubMed2002

Information processing in social phobia.

Cognitive theories suggest that information processing biases play a central role in the development and maintenance of emotional disorders. The present article reviews recent studies of information processing biases in social phobia and considers the significance of the findings for understanding the persistence of the condition. Taken together, the studies suggest that social phobia is characterized by biases in the following: interpretation of external social events; detection of negative responses from other people; the balance of attention between external and self-processing; the use of internal information to make inferences about how one appears to others; recall of negative information about one's perceived, observable self; and by a variety of problematic anticipatory and post-event types of processing. If such biases play a role in maintaining social anxiety, experimental manipulation of the biases should modulate anxiety responses. Several recent studies have confirmed this prediction, but further research is required. Methodological limitations of existing information processing studies are highlighted. Finally, possible neurobiological correlates are discussed and suggestions are made for future attempts to link neurobiology and cognitive psychology.

Attention↗
PubMed1980

Nonaphasic misnaming and other neurobehavioral features of an unusual toxic encephalopathy: case study.

A patient with propranolol-induced mental status changes was studied during and after the period of propranolol intoxication. While intoxicated he manifested the syndrome of "non-aphasic misnaming," did poorly on the nonverbal portions of the WAIS, and exhibited perseveration and variability of performance. Our observations clarify the nature of the neurobehavioral disturbances in toxic-metabolic encephalopathies.

Aged↗
PubMed2005

[False recognition of faces associated with fronto-temporal dementia with prosopagnosia].

INTRODUCTION: The association of prosopagnosia and false recognition of faces is unusual and contributes to our understanding of the generation of facial familiarity. METHOD: A 67-year-old man with a left prefrontal traumatic lesion, developed a temporal variety of fronto-temporal dementia (semantic dementia) with amyotrophic lateral sclerosis. Cerebral imagery demonstrated a bilateral, temporal anterior atrophy predominating in the right hemisphere. The main cognitive signs consisted in severe difficulties to recognize faces of familiar people (prosopagnosia), associated with systematic false recognition of unfamiliar people. RESULT: Neuropsychological testing indicated that the prosopagnosia probably resulted from the association of an associative/mnemonic mechanism (inability to activate the Face Recognition Units (FRU) from the visual input) and a semantic mechanism (degradation of semantic/biographical information or deconnexion between FRU and this information). At the early stage of the disease, the patient could activate residual semantic information about individuals from their names, but after a 4-year course, he failed to do so. This worsening could be attributed to the extension of the degenerative lesions to the left temporal lobe. Familiar and unfamiliar faces triggered a marked feeling of knowing. False recognition concerned all the unfamiliar faces, and the patient claimed spontaneously that they corresponded to actors, but he could not provide any additional information about their specific identities. The coexistence of prosopagnosia and false recognition suggests the existence of different interconnected systems processing face recognition, one intended to identification of individuals, and the other producing the sense of familiarity. Dysfunctions at different stages of one or the other of these two processes could result in distortions in the feeling of knowing. CONCLUSION: From this case and others reported in literature, we propose to complete the classical model of face processing by adding a pathway linked to limbic system and frontal structures. This later pathway could normally emit signals for familiarity, essentially autonomic, in response to the familiar faces. These signals, primitively unconscious, secondly reach consciousness and are then integrated by a central supervisor system which evaluates and verifies identity-specific biographical information in order to make a decision about the sense of familiarity.

Aged↗
PubMed2003

Neurobehavioral effects of pesticides: state of the art.

The authors have reviewed the literature on neurobehavioral toxicity of pesticides to assess the status of knowledge on this matter. Some data suggest that exposure to DDT and fumigants may be associated with permanent decline in neurobehavioral functioning and increase in psychiatric symptoms, but, due to the limited number of studies available and the scarce knowledge on exposure levels, no firm conclusion can be drawn. Data on subjects acutely poisoned with organophosphorous compounds suggest that an impairment in neurobehavioral performance and, in some cases, emotional status may be observed as a long-term sequela, but the possibility still remains that these effects were only an aspecific expression of damage and not of direct neurotoxicity. Studies carried out on subjects chronically exposed to organophosphates, but never acutely poisoned, do not provide univocal results but the slight changes consistently observed in sheep dippers suggest the need of focusing on activities characterized by relatively higher exposure levels. In general, the main limits of existing knowledge are the variability of the testing methods used, which makes it difficult to compare the results of single studies, and the scarce knowledge on exposure levels. A promising approach may be the conduction of prospective longitudinal or cohort studies, where exposure and dose assessment can be more easily controlled, or the evaluation of cohorts of workers a priori selected for the availability of environmental and biological monitoring data. The follow up of the populations under study may give an answer at the problem of the prognostic significance of the observed changes. Also the protocols used to assess neurobehavioral functioning need to be standardized.

Animals↗
PubMed2004

Cognitive and neurological impairment in mood disorders.

Disorders of mood are accompanied by a range of cognitive and neurological impairments. Similar types of cognitive deficits are shared by patients with unipolar depression and bipolar disorder. Given the disparate clinical nature of these two disorders, it is interesting and informative to understand that they share common impairments in cognition. Neuro-imaging studies indicate that these impairments in both patient populations may be subserved by disruptions of the dorsal lateral and ventral medial PFC. An important problem that remains for clinicians is that some neurological symptoms are linked specifically to the adverse pharmacological effects of antidepressant agents, mood stabilizers, and neuroleptic agents. Research has shown a relation between mood and cognitive ability. Studies also have shown an association between mood and specific types of neurological dysfunction. Although few studies have examined all three symptom domains within one investigation, preliminary reports indicate that mood, cognition, and motor function may be linked to one another by complex mechanisms. Moreover, either type of abnormality that persists in the euthymic state suggests that a fundamental neural dysfunction is unaffected by treatment with existing means. Understanding the neural mechanisms that underlie mood, cognition, and movements may help to devise better treatments that do not influence cognitive or neurological functions,yet treat mood successfully.

Attention↗
PubMed2004

Cognitive and neurobiological findings in obsessive-compulsive disorder.

The behavioral disturbances seen in OCD patients likely are related to abnormalities in the frontal striatal systems, with complex involvement of other brain regions. This is suggested by data from various modalities. Executive deficits are seen on neuropsychological assessments, which may contribute to poor performance on tasks designed to test other domains. Studies of neurological illness in which obsessive and compulsive symptoms are seen with increased frequency and results of neuroimaging studies are also indicative of frontal-striatal dysfunction. Some neuroimaging studies specifically implicate the OFC, along with other regions such as the anterior cingulate cortex and caudate nucleus. Data from studies of neurological soft signs are less specific and suggest pathology that may be common to other psychiatric conditions, such as schizophrenia. Although data from these various modalities do not give clear guidance on treatment, future work may show usefulness of adding these assessments to a clinical evaluation,especially with respect to predicting treatment response in subtypes of OCD.

Brain↗
PubMedDate not supplied

Executive deficits appearing in the initial stage of Alzheimer's disease.

The presence of executive deficits has been sought at a stage of Alzheimer's disease where currently used neuropsychological batteries could not yet distinguish Alzheimer's patients from normal age- and education-matched controls. This study shows that, at this early stage, those patients that 6 months later are found to show clear signs of Alzheimer's had been significantly worse than normal controls in an executive function task adapted from the Brown-Peterson procedure.

Adult↗
PubMed1997

Context memory in schizoaffective and schizophrenic disorders.

DSM IV preserves the boundary between schizoaffective disorder and schizophrenia, yet validation of the former condition remains incomplete. The prevalent view that schizoaffective disorder is a less serious condition than schizophrenia suggest that cognitive disturbance might be less severe and possibly different from that found in schizophrenia. We investigated a well-characterized cognitive difficulty in schizophrenia, the relative lack of gain in verbal recall when context is increased, in samples of patients and normal controls. Subjects with schizophrenia (n = 19) were individually matched for age, sex, and recall performance with patients diagnosed with schizoaffective disorder (n = 19) and major depression (n = 19); and with normal controls (n = 19). Patients were also matched on duration of illness. The results indicate that schizophrenic subjects attain smaller gains in recall when context is increased compared to depressed and normal controls, a finding consistent with previous results. Schizophrenic and schizoaffective subjects, however, did not differ in recall gain on this task. We conclude that schizoaffective subjects cannot be distinguished from schizophrenic subjects on this cognitive feature.

Adult↗
PubMed1999

Object identification deficits in dementia of the Alzheimer type: combined effects of semantic and visual proximity.

Identification deficits in dementia of the Alzheimer Type (DAT) often target specific classes of objects, sparing others. Using line drawings to uncover the etiology of such category-specific deficits may be untenable because the underlying shape primitives used to differentiate one line drawing from another are unspecified, and object form is yoked to object meaning. We used computer generated stimuli with empirically specifiable properties in a paradigm that decoupled form and meaning. In Experiment 1 visually similar or distinct blobs were paired with semantically close or disparate labels, and participants attempted to learn these pairings. By having the same blobs stand for semantically close and disparate objects and looking at shape-label confusion rates for each type of set, form and meaning were independently assessed. Overall, visual similarity of shapes and semantic similarity of labels each exacerbated object confusions. For controls, the effects were small but significant. For DAT patients more substantial visual and semantic proximity effects were obtained. Experiment 2 demonstrated that even small changes in semantic proximity could effect significant changes in DAT task performance. Labeling 3 blobs with "lion," "tiger," and "leopard" significantly elevated DAT confusion rates compared to exactly the same blobs labeled with "lion," "tiger," and "zebra." In conclusion both visual similarity and semantic proximity contributed to the identification errors of DAT patients.

Aged↗
PubMed1999

Brain mapping of language and auditory perception in high-functioning autistic adults: a PET study.

We examined the brain organization for language and auditory functions in five high-functioning autistic and five normal adults, using [15O]-water positron emission tomography (PET). Cerebral blood flow was studied for rest, listening to tones, and listening to, repeating, and generating sentences. The autism group (compared to the control group) showed (a) reversed hemispheric dominance during verbal auditory stimulation; (b) a trend towards reduced activation of auditory cortex during acoustic stimulation; and (c) reduced cerebellar activation during nonverbal auditory perception and possibly expressive language. These results are compatible with findings of cerebellar anomalies and may suggest a tendency towards atypical dominance for language in autism.

Adolescent↗