Physician, Entrepreneur, Teacher, Researcher, Consultant

Dr. Dan Miulli

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Alzheimer's disease (AD) is chronic with a gradual decrease in attention span, visuospatial orientation, and activities of daily living plus depression, agitation, illusions, hallucinations, and mood change. However, the most physiologically significant change is associated with memory. Specifically, the lesions in AD are located close to both the anatomic region of glutamate-mediated memory and the region of specific loss of glutamatergic innervation.1-3 Glutamate has many potential precursors and metabolites, the result being a possibility for error in its production and conceivable neurotoxic effects. In search of a predictive test for AD, it is therefore logical to measure these precursors and metabolites of glutamate. In fact, the loss of glutamatergic innervation has been studied extensively from homogenized tissue in AD patients postmortem,3 and an abnormal glutamate concentration has been found in these tissues.
Clearly, it is time-consuming and expensive to rule out treatable causes of dementia. Tissue analysis is costly, inaccurate, and inappropriate for analyzing a large number of living patients. Furthermore, in the event that a cure might be discovered, there will be need for an economical diagnostic tool that creates little morbidity. This pilot study shows that analysis of some plasma metabolites of glutamate may serve as such a tool.

Methods
Twenty-six participants were entered into this pilot study. The 14 persons in the control group (age range, 61 to 96 years; average age, 80 years) con-sisted of 4 men and 10 women. The 12 patients in the AD group (age range, 70 to 89 years; average age, 81 years) consisted of 1 man and 11 women. These patients had moderate to severe AD. All the participants were selected from one nursing home population, were ambulatory or able to walk (not completely bedridden), and were not cachectic but well nourished without weight changes and on different diet regimens.
A total of 197 patients were screened to exclude the following: those who had other causes of dementia, such as neurodegenerative disorders, normal-pressure hydrocephalus, centeral nervous system (CNS) infections, metabolic disorders, mass lesions, or multi-infarct dementia; those taking neuroleptic or other CNS-active drugs; patients with acute myocardial infarction, endocrine disorders, history of toxic ingestion, nutritional diseases, malnourishment, liver disease, biliary obstruction, pancreatitis, Reye's syndrome, muscle trauma, intestinal injury or trauma, burns, severe diabetes, olivopontocerebellar atrophy, or psychiatric illness and depression; or those who had deviations from the normal values for erythrocyte sedimentation rate, serum alanine and aspartate transaminases, y-glutamyl transferase, or other tests in conjunction with the aforementioned afflictions. Those who passed the exclusion criteria

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Dr. Miulli Home Page

Selected Works Page

CORAL CHIP ALLOGRAFT FUSION FOR ACD

COMPUTERIZATION IN MEDICINE

BLOOD BRAIN BARRIER

ECCRINE EPITHELIOMA

TIME & GRAVITY

ELDERLY LUMBAR SURGERY

DISK CHANGES WITH AGING

INDICATIONS FOR FUSION

NEUROSCIENCE CENTER

CRYOSURGERY

GBM MOLECULAR TARGETS

VASOSPASMS

ELECTROPHYSIOLOGICAL MONITORING IN SURGERY

SPECTROSCOPY OF TUMORS

GLUTAMATE IN ALZHEIMER'S

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