Treatment of dementia-associated agitation with gabapentin.

The authors describe the use of gabapentin in the treatment of 4 outpatients with dementia-associated agitation. On the basis of clinical case reports and the Overt Agitation Severity Scale, all 4 patients had reduced agitation with gabapentin. Three of 4 patients were successfully titrated to a full dose of 2,400mg/day. These findings suggest a possible role for gabapentin in the behavioral management of patients with dementia.

Neuropsychological characteristics of subjects with and without neocortical Alz-50 immunoreactivity.

We performed quantitative histopathology and Alz-50 staining on 8 non-demented and 16 demented subjects who had received yearly neuropsychological evaluations as part of prospective studies of dementia. Of the 8 non-demented subjects, four had begun to show signs of cognitive decline on serial neuropsychological testing. These subjects showed marked decline on the Fuld Object Memory Evaluation, a test of recent memory. Scores on IQ tests and the Blessed test of orientation, memory, and concentration showed fluctuations but not consistent declines. These old-old, retired subjects were called "cognitively impaired" but not demented because they did not show decline in activities of daily living or social interactions. Five of the non-demented subjects had numerous cortical senile plaques and met standard pathological criteria for Alzheimer's disease (AD), but only one of the five was Alz-50 positive. That subject had shown the most consistent decline on neuropsychological scores. Ten of 11 clinically demented subjects with pathological evidence of AD were Alz-50 positive. All five clinically demented subjects with non-Alzheimer dementias on pathological examination were Alz-50 negative. Alz-50 may stain plaques found in AD, but not stain plaques which accompany aging. The cognitive impairment found in the Alz-50 negative subjects may be age-associated and not indicate early AD.

Reexpression of a developmentally regulated antigen in Down syndrome and Alzheimer disease.

ALZ-50 is a monoclonal antibody that recognizes a protein of apparent molecular mass 68 kilodaltons (A68). The protein is present in the brains of patients with Alzheimer disease but is not detectable in normal adult brain tissue. We now report that ALZ-50-reactive neurons are found in normal fetal and neonatal human brain and in brain tissue from neonatal individuals with Down syndrome. Reactive neurons decrease sharply in number after age 2 and reappear in older individuals with Down syndrome and in patients with Alzheimer disease.

Characterization of monoclonal antibodies to galactolipids and uses in studies of dementia.

A panel of monoclonal antibodies was prepared from mice immunized with homogenates of ventral forebrain from patients with Alzheimer's disease (AD). The cortex and hippocampus which receive cholinergic innervation from the ventral forebrain have been reported to demonstrate a greater number of neuritic plaques and neurofibrillary tangles. With an enzyme-linked immunosorbent assay (ELISA), two of these antibodies reacted with chloroform/methanol soluble antigens. Folch extraction and partition followed by silicic acid column chromatography revealed the antigens to be glycolipids. Studies with a variety of purified lipids revealed that the antibodies reacted with galactosyl sphingosine, cerebrosides and sulfatides. These antibodies have been used to examine galactosphingolipids in brains with AD with both quantitative ELISA and immunocytochemical techniques. Additionally, the galactolipid composition of Pick's disease has also been studied using these antibodies.

Marked loss of cerebral galactolipids in Pick's disease.

Studies with two monoclonal antibodies reactive with galactolipids suggest that there is a marked loss of these compounds in the brains of patients with Pick's disease. Quantitative assays, immunocytochemical studies, and thin-layer chromatography confirm that both galactocerebrosides and sulfatides are selectively lost in this condition. This finding appears to be specific for Pick's disease, distinguishing it from Alzheimer's disease and other dementing disorders.