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Biomedical subjects

M Mesulam

Publications and source records attributed to M Mesulam.

8 recordsLinked to original sources
PubMed1994

A potential noninvasive neurobiological test for Alzheimer's disease.

Currently Alzheimer's disease, which affects more than 20 million people worldwide, can only be definitely diagnosed by histological examination of brain tissue obtained at autopsy or biopsy. There is a great need for an early, noninvasive, sensitive, and easily administered diagnostic test of Alzheimer's disease. Here it is reported that patients diagnosed with probable Alzheimer's disease by standard clinical criteria exhibited a marked hypersensitivity in their pupil dilation response to a cholinergic antagonist, tropicamide, placed in their eyes. It was possible to distinguish 18 of 19 individuals (95%) either clinically diagnosed with Alzheimer's disease or classified as suspect Alzheimer's individuals by neuropsychological screening from 30 of 32 normal elderly controls (94%).

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PubMed1992

Cholinesterases in the amyloid angiopathy of Alzheimer's disease.

Vessels affected by amyloid angiopathy in patients with Alzheimer's disease also displayed intense acetylcholinesterase and butyrylcholinesterase activity when examined by light and electron microscopy. The enzymatic properties of the vessel-bound cholinesterases were identical to those of the cholinesterases associated with senile plaques and neurofibrillary tangles. This cholinesterase activity is of unknown origin but represents one of the very few features common to all the major pathological markers of Alzheimer's disease.

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PubMed1991

Differential distribution of a neurofilament protein epitope in acetylcholinesterase-rich neurons of human cerebral neocortex.

The majority of acetylcholinesterase-rich pyramidal neurons in neocortical layers III and V of the human brain displayed intense immunostaining with SMI-32, a monoclonal antibody which recognizes a non-phosphorylated epitope of neurofilament proteins. In contrast, very few of the heteromorphic acetylcholinesterase-rich perikarya embedded in the white matter of the cerebral hemispheres are associated with this type of immunostaining. These two groups of acetylcholinesterase-rich cortical neurons can thus be differentiated not only on the basis of morphology and location but also on the basis of cytochemical signature. The concurrent visualization of SMI-32 immunoreactivity and acetylcholinesterase enzyme activity also showed that SMI-32 immunoreactive neurons can be subdivided into several subgroups on the basis of their perikaryal acetylcholinesterase activity.

Acetylcholinesterase↗
PubMed1990

Competitive substrate inhibition in the histochemistry of cholinesterase activity in Alzheimer's disease.

We used acetylcholine and butyrylcholine to competitively inhibit the cleavage of acetylthiocholine or butyrylthiocholine in plaques and tangles of Alzheimer's disease. Butyrylcholine was much more effective than acetylcholine in reducing the histochemical reaction for acetylcholinesterase not only in neuronal fibers, but also in plaques and tangles. This is in keeping with biochemical data on acetylcholinesterase and supports the existence of true acetylcholinesterase activity within plaques and tangles. However, 2-4 times higher acetylcholine and buturylcholine concentrations were necessary to inhibit the plaque and tangle bound enzyme. Together with the previously reported different pH optima, this suggests that the plaque- and tangle-bound acetylcholinesterase may represent an altered form of this enzyme.

Acetylcholinesterase↗
PubMed1989

Special properties of cholinesterases in the cerebral cortex of Alzheimer's disease.

Selective cholinesterase inhibitors such as BW284C51 and iso-OMPA showed that the plaques and tangles of Alzheimer's disease contain acetylcholinesterase and butyrylcholinesterase activity. In comparison to the cholinesterases of the normal brain, the plaque and tangle-bound cholinesterases in Alzheimer's disease display major shifts in optimum pH and inhibitor sensitivity.

Acetylcholinesterase↗
PubMed1985

Psychiatric manifestations of right hemisphere infarctions.

Five right-handed patients (aged 45 to 78 years) developed acute psychotic disturbances in conjunction with infarcts in the right hemisphere. Their presentation was marked by agitation, inattention, suspiciousness, paranoid delusions, hallucinations, and lack of appropriate concern. Several of these patients initially received primary psychiatric diagnoses. Although neurological findings indicative of right hemisphere involvement could also be elicited, these were generally overshadowed by the more dramatic behavioral alterations. The electroencephalogram and computerized axial tomography were positive in most cases. These cases demonstrate that the possibility of a right hemisphere lesion needs to be entertained in patients who present with an atypical psychotic episode.

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PubMedDate not supplied

Neurocognitive networks and selectively distributed processing.

The association cortex of the human brain can be divided into unimodal and transmodal components. Unimodal (modality-specific) cortical areas are subdivided into upstream regions specialized for encoding unitary features of experience and downstream regions which are specialized for encoding composite features. Modality-specific features lead to multimodal knowledge through the mediation of transmodal areas in the brain. These transmodal areas include cortical regions that are conventionally designated as heteromodal, paralimbic and limbic cortex. Contrary to earlier formulations, it is no longer thought that these transmodal areas contain a convergent residue of knowledge. Instead, it appears that the role of these transmodal areas is to contain a road map for the multifocal binding and calling up of distributed information in multiple modalities. Knowledge can thus be encoded in a flexible distributed rather than rigid convergent form. Observations on patients with focal neurological lesions indicate that transmodal areas act like neural hubs (or gateways) for accessing critical domains of knowledge rather than as dedicated centers for specific cognitive functions. In the processes related to memory, a limbic structure such as the hippocampus does not act as a bank for specific memories but as a critical node for accessing distributed information related to recently acquired experience. Damage to a sufficient volume of the limbic system interferes with the coherence of recall and storage even though the constituent fragments of the corresponding experiences may remain stored quite well in other parts of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Cortex↗