US scientists discuss early detection and treatment of Alzheimer’s diseaseBMJ 2012; 344 doi: https://doi.org/10.1136/bmj.e1068 (Published 13 February 2012) Cite this as: BMJ 2012;344:e1068
The US president, Barack Obama, has announced an increase in funding for Alzheimer’s disease next year of $106m (£67m; €80m), a 24% rise over the current $450m a year.
The announcement came shortly after scientists gathered at a meeting of the New York Academy of Sciences in New York to try to determine how best to spot Alzheimer’s disease in the “silent years” before the disease is apparent.
Reisa Sperling, director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital, Boston, said, “The pathophysiology begins more than a decade before dementia . . . We are trying to define the earliest markers for the ‘iceberg’ silent years when preclinical changes are occurring . . . We need to intervene earlier.”
She proposed three stages before the appearance of Alzheimer’s disease: asymptomatic amyloidosis (accumulation of amyloid plaques in the brain); amyloidosis with neurodegeneration; and amyloidosis with neurodegeneration and subtle cognitive impairment. She said that it might take 15 years between the accumulation of amyloid plaques and the emergence of symptomatic disease. How much amyloid accumulates and the rate of accumulation seem related to the rate of mental decline, she said.
She told the BMJ that about a third of elderly patients who were judged to be clinically normal at interview and by cognitive testing had amyloid plaques similar to those in Alzheimer’s patients.
“Not everyone [with amyloid plaques] progresses to Alzheimer’s, but if we could delay its onset by five years we would cut the costs for dementia to Medicare [the health insurance programme for elderly people] by 50%,” she said. About five million adults in the United States have Alzheimer’s disease.
John Morris, of Washington University School of Medicine in St Louis, said that beginning treatment when symptoms had appeared was too late. Amyloid plaques were present in about 20% of clinically normal people in their 60s, 25% of people in their 70s, and 30% of people in their 80s, he said. Patients with mild cognitive impairment who died from causes such as a myocardial infarction or a car crash were found to have lost up to 60% of neuronal cells.
Accumulation of amyloid plaques is not the only known risk factor for Alzheimer’s disease, however. People who are carriers of the apolipoprotein E gene are at increased risk, and other factors may play a role, speakers said.
Brian Gold, of the University of Kentucky, said that in addition to the amyloid plaques and neurofibrillary tangles associated with Alzheimer’s, there was new evidence of microstructural changes affecting the brain’s white matter very early in the disease, which indicates that there may be several pathways to the development of Alzheimer’s disease.
Dr Morris commented: “People are starting to ask about tests.” At present, tests of cerebrospinal fluid are available, costing about $900; some private insurance companies will pay for them.
Simon Lovestone, professor of old age psychiatry at the London academic health science centre King’s Health Partners, told the BMJ that there was “a possibility—no more—of a biomarker for preclinical disease.” He said many markers seem to fall along the complement pathway, but no preclinical marker was ready for routine use, although a biomarker might be useful to test the effectiveness of potential disease modifying agents in clinical trials. He said, “Any test has the potential to alarm the worried well, and that is why we should exercise appropriate caution before the introduction of any test.”
Cite this as: BMJ 2012;344:e1068
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