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D Dickson

Publications and source records attributed to D Dickson.

At least 127 records · Page 7Linked to original sources
PubMed1997

Pathological diagnostic criteria for dementia associated with cortical Lewy bodies: review and proposal for a descriptive approach.

In recent years dementia histologically characterised by the presence of cortical Lewy bodies has been increasingly recognised. There is now need for a scheme for an internationally acceptable scheme for pathological diagnosis and classification so that clinical, pathological and molecular features of disease can be correlated. Recent observations made by different groups in large patient series have used slightly different pathological criteria resulting in at least seven different diagnostic terms. In some patients the only cortical pathology is the presence of Lewy bodies, while in the majority of patients there are coexisting pathological changes which either overlap with those seen in Alzheimer's disease (AD). Cortical Lewy bodies can also be present in patients who do not have any obvious cognitive abnormality. A problem with equating studies from different groups is that different criteria have been used to define AD, so that establishing the relevance of cortical Lewy bodies themselves to cognitive decline and separating this from the contribution which may be related to the AD pathology is problematic. The lesions which appear to be of most relevance to potential cognitive decline in DLB are cortical Lewy bodies, Lewy-related neurites, senile plaques, neurofibrillary tangles, neuronal and synaptic loss, spongiform change, and cortical cholinergic deficits. It is possible to operationally classify patients with cognitive decline and cortical Lewy bodies into three main groups, Cortical Lewy body disease, Cortical Lewy body disease with plaques, and Cortical Lewy body disease with plaques and tangles. There are frequent cases which overlap these groups making operational classification difficult in practice. A descriptive classification, in which the severity of different pathological changes is rated, is easy to use in practice. As new molecular risk factors for AD or DLB are revealed they will need to be related to morphological and clinical features. A descriptive diagnostic assessment for DLB will facilitate such studies and makes no judgements as to what these relationships will be.

Aged↗
PubMed1997

Distribution and subcellular localization of high-molecular-weight microtubule-associated protein-2 expressing exon 8 in brain and spinal cord.

The expression of high-molecular-weight (HMW) microtubule-associated protein-2 (MAP-2) expressing exon 8 (MAP-2 + 8) was examined by immunoblotting during rat brain development and in sections of human CNS. In rat brain, HMW MAP-2 + 8 expression was detected at embryonic day 21 and increased during postnatal development. In adult rats, HMW MAP-2 + 8 comigrated with MAP-2a. In human adult brain, HMW MAP-2 + 8 was expressed in select neuronal populations, including pyramidal neurons of layers III and V of the neocortex and parahippocampal cortex, pyramidal neurons in the endplate, CA2 and subiculum of the hippocampus, and the medium-sized neurons of the basal ganglia. In the cerebellum, a subpopulation of Golgi neurons in the internal granular cell layer and most Purkinje cells were also stained. In the spinal cord staining was observed in large neurons of the anterior horn. Staining was present in cell bodies and dendrites but not in axons. At the ultrastructural level, HMW MAP-2 + 8 immunoreactivity was observed on mitochondrial membranes and in postsynaptic densities (PSDs) of some asymmetric synapses in the midfrontal cortex and spinal cord. Immunoblots of proteins isolated from enriched mitochondrial and PSD fractions from adult human frontal lobe and rat brains confirmed the presence of HMW MAP-2 + 8. The presence of HMW MAP-2 + 8 in dendrites and in close proximity to PSDs supports a role in structural and functional attributes of select excitatory CNS synapses.

Amino Acid Sequence↗
PubMed1997

Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects. A retrospective postmortem immunocytochemical and histofluorescent study.

Diabetics have impaired cognitive performance relative to age-matched control subjects, but the pathologic basis for this impairment is unknown. Because Alzheimer-type lesions, including both senile plaques and neurofibrillary tangles, contain glycated proteins and glycation is known to be increased in diabetes, we hypothesized that cognitive impairment in diabetes may be due in part to increased Alzheimer-type pathology. We measured the amount of Alzheimer-type pathology in postmortem brains of diabetic and age-matched control subjects with sensitive and specific histofluorescent and immunocytochemical methods. As expected, there were strong correlations between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between the pathologic measures. On the other hand, there was no significant difference between diabetics and control subjects with respect to severity of Alzheimer-type pathology, on average, or with respect to age. This finding was true for diabetics with and without insulin dependence. The results confirm reports showing that diabetes is not a risk factor for Alzheimer-type pathology and suggest that factors other than Alzheimer's disease are responsible for cognitive impairment in diabetics.

Age Distribution↗
PubMed1996

For medicinal purposes.

Developments in techniques of pharmaceutical chemistry are poised to revolutionize the design of drugs beyond previous expectations. But what are our current expectations and what does the future hold?

Chemistry, Pharmaceutical↗