Alzheimer’s disease researchers held an extended study on family of 5,000 people in Colombia and found out that brain deterioration begins earlier than it is widely known.
According to the new study released in the journal Lancet Neurology, researchers found symptoms of mild brain deterioration as early as 18 years old. The mild brain changes began as least 20 years before in the most cases.
Dr. Eric Reiman (Banner Alzheimer’s Institute in Phoenix) and Dr. Francisco Lopera (University of Antioquia) received a grant to test a drug on younger Columbian family members to see if the drug can slow or stop the brain deterioration.
Dr. Reiman said, “The prevailing theory has been that development of Alzheimer’s disease begins with the progressive accumulation of amyloid in the brain. This study suggests there are changes that are occurring before amyloid deposition.”
The other possibility is that the brain is already impaired genetically.
In one of the Lancet Neurology studies, researchers examined 44 relatives between ages 18 to 26. Twenty had the mutation that causes Alzheimer’s. The cerebrospinal fluid of those with the mutation contained more amyloid than that of relatives without it. This was striking because researchers know that when people develop amyloid plaques — whether they have early-onset or late-onset Alzheimer’s — amyloid levels in their spinal fluid are lower than normal. That is believed to be because the fluid form of amyloid gets absorbed into the plaque form, Dr. Reiman said.
So, the high level of amyloid fluid in the Colombian family supports a hypothesis about a difference between the beginning phases of genetic early-onset Alzheimer’s and the more common late-onset Alzheimer’s. The difference may be that early-onset Alzheimer’s involves an overproduction of amyloid, while late onset involves a problem clearing amyloid from the brain.
In another result, when the subjects performed a task matching names with faces, those with the mutation had greater activity in the hippocampus and parahippocampus, areas involved in memory. Dr. Reiman suggested this could mean that the pre-Alzheimer’s brain has to expend more effort to encode memories than a normal brain.
Researchers also found that the mutation carriers had less gray matter in areas that tend to shrink when people develop dementia. Dr. Fox emphasized that seeing less gray matter so early was so novel that it should be treated cautiously unless other studies find a similar result.
The second study intensively focused on 50 people from the family ages ranging from 20 to 56 years old. 11 had dementia and 19 had mutation carriers. The rest of 20 members were normal. Brain imaging held by 50 subjects showed that amyloid plaques began around 28 years of age, or at least 15 years before the outbreak.
Currently the group of researchers led by Dr. Reiman and Dr. Lopera began studying on family members aging from 7 to 17 to see the deterioration begins even earlier than found.
(Content credit: New York Times/ Journal Lancet Neurology)
reporter
Park Sae-jin
swatchsjp@ajunews.com