Progression of clinical deterioration and pathological changes in patients with Alzheimer disease evaluated at biopsy and autopsy.

Objectives: To quantify the progression of senile plaques, neurofibrillary tangles, cerebral amyloid angiopathy, and microglial activation in the cortex and white matter of patients with Alzheimer disease evaluated at both biopsy and subsequent autopsy and correlate these changes with the progression of neurologic impairment.

Setting: Academic referral center for patient with Alzheimer disease.

Patients: Four patients meeting the clinical criteria for Alzheimer disease, enrolled in a pilot study for the evaluation of response to intracerebroventricular administration of bethanechol chloride.

bcl-2 expression decreases methyl mercury-induced free-radical generation and cell killing in a neural cell line.

Methyl mercury neurotoxicity is associated with a broad range of neuropathologic and biochemical disturbances which include induction of oxidative injury. Treatment of the hypothalamic neural cell line GT1-7 with 10 microM methyl mercury (MeHg) for 3 h resulted in increased formation of reactive oxygen species (ROS), and decreased levels of reduced glutathione (GSH), associated with 20% cell death. Cells transfected with an expression construct for the anti-apoptotic proto-oncogene, bcl-2, displayed attenuated ROS induction and negligible cell death.

Rapid cell death induced by methyl mercury in suspension of cerebellar granule neurons.

We have further investigated the cytotoxicity of methyl mercury (MeHg) in cerebellar granule neurons isolated from 5-12-day-old rats. At 20 microM MeHg adenosine triphosphate (ATP) levels were reduced to 30% of control within 15 minutes and 1% of control at three hours (h), while cell viability assayed by trypan blue exclusion was reduced to approximately 80% and 20% of control, respectively. When potassium cyanide (KCN) was used to reduce ATP levels greater than 95%, virtually no change in cell viability was observed during three h incubation.

Abnormalities of peripheral nerve in patients with human immunodeficiency virus infection.

The purpose of this study was to assess systematically morphology of peripheral nerves from patients with human immunodeficiency virus infection (acquired immunodeficiency syndrome [AIDS] and AIDS-related complex) examined at autopsy. Sural nerve specimens were taken from 25 patients (mean age 44 years) and evaluated by routine procedures used in our laboratory. In 13 cases no detectable abnormality was seen.