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High doses of vitamins may help slow the progression of Alzheimer's disease. That's the finding of a pilot study in the March/April issue of the American Journal of Geriatric Psychiatry.
Researchers at the Georgetown University Medical Center's Memory Disorders Program found high-dose vitamins reduce levels of the amino acid homocysteine in people with Alzheimer's. Previous research has found a link between homocysteine and the mind-robbing disease.
The Georgetown University researchers are now leading a 40-center therapeutic trial to determine whether three common vitamins -- folic acid, B12 and B6 -- can decelerate Alzheimer's.
The study, funded by the U.S. National Institute on Aging, has started recruiting 400 people with mild to moderate Alzheimer's disease. They'll be randomly assigned to receive either vitamins or placebos.
Their cognitive function -- memory, thinking and language -- will be assessed over the course of 18 months to determine the progress of their disease.
Anyone in the Washington, D.C., area interested in enrolling a family member with mild to moderate Alzheimer's disease in the trial at Georgetown University can contact the Memory Disorders Program at 202-784-6671.
Alzheimers
Alzheimer's disease (AD), a neurodegenerative disorder, is the most common cause of dementia and characterised clinically by progressive intellectual deterioration together with declining activities of daily living and neuropsychiatric symptoms or behavioral changes.
The most striking early symptom is memory loss (amnesia), usually manifest as minor forgetfulness that becomes steadily more dense with illness progression, with relative preservation of older memories.
As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), coordinated movement (apraxia), recognition (agnosia) and those functions (such as decision-making and planning) closely related to the frontal lobe of the brain, reflecting extension of the underlying pathological process.
This consists principally of neuronal (cell) loss (or atrophy), together with deposition of amyloid plaques and neurofibrillary tangles. Genetic factors are known to be important, and polymorphisms (variations) in three different autosomal dominant genes - Presenilin 1, Presenilin 2, and A-Beta - have been identified that account for a small number of cases of familial, early-onset AD.
For late onset AD (LOAD), only one susceptibility gene has so far been identitified - the epsilon 4 allele of the APOE gene. Age of onset itself has a heritability of around 40%.