Medical College of Wisconsin researchers in Milwaukee have reported that children of Alzheimer's patients who are carriers of a genetic risk factor for Alzheimer's disease have neurological changes that are detectable long before clinical symptoms may appear.
Functional MRI brain imaging revealed that these symptomless carriers of the APOE-4 gene demonstrated significantly reduced functional brain connectivity between the hippocampus and the posterior cingulated cortex, two important brain structures for memory processing. These structures are relevant for information acquisition, filtering and sorting.
The study, conducted at Froedtert Hospital, was led by Shi Jiang Li, Ph.D., professor of biophysics, and was presented at the Alzheimer's Association International Conference on Alzheimer's disease in Chicago, July 29th.
"Just as if cancer could be detected when there were only a few cells, decades before it was evident, the advantage of identifying those at great risk for having Alzheimer's would be of tremendous value in development of interventional therapies," says Dr. Li.
The researchers studied 28 neurologically-normal subjects, between ages 45 and 65. Twelve carried the APOE-4 gene and 16 did not. The two groups showed no significant difference in age, educational level, or neuropsychological performances. All subjects received fMRI scans. For each subject, functional connectivity between the two brain structures was measured in a resting state.
Results showed that functional connectivity in the non APOE-4 carriers was approximately 65 percent better than that of the carriers.
Source: Medical College of Wisconsin
Related stories:
How the APOE gene can modify your risk for Alzheimer's disease
One of the hallmarks of the brain of an individual with Alzheimer disease is the accumulation of amyloid-beta peptide (A-beta), something that is believed to be toxic to many brain cells (specifically neurons) and to therefore contribute to the underlying cause of disease. Berislav Zlokovic and colleagues, at the University of Rochester Medical School, have now generated data in mice that mechanistically links a genetic risk factor for Alzheimer disease with accumulation of A-beta in the brain.
Mechanism explains link between apolipoprotein E and Alzheimer's disease
Scientists have discovered a previously unknown mechanism by which apolipoprotein E, a molecule whose mutation is linked to Alzheimer's disease (AD), stimulates degradation of sticky amyloid beta (A-beta) protein within the brain. The research, published by Cell Press in the June 12 issue of the journal
Neuron, may lead to a powerful new therapy for this devastating disease.
Diabetes in mid-life linked to increased risk of Alzheimer's disease
Men who develop diabetes in mid-life appear to significantly increase their risk of developing Alzheimer’s disease, according to a long-term study published in the April 9, 2008, online issue of
Neurology, the medical journal of the American Academy of Neurology.
Engineered mice provide insight into Alzheimer's disease
One factor that determines how at risk an individual is of developing late-onset Alzheimer disease (AD) is the version of the APOE gene that they carry — those carrying the gene that enables them to make the apoE4 form of the apoE protein are at increased risk and those carrying the gene that enables them to make the apoE2 form are at decreased risk.
Evidence found for genes that affect risk of developing Alzheimer's disease
Through one of the largest studies yet of Alzheimer’s disease (AD) patients and their brothers, sisters, and children, researchers at Mayo Clinic Jacksonville have found strong evidence that genes other than the well-known susceptibility risk factor APOE4 influence who is at risk for developing the neurodegenerative disease later in life.
Linking 2 molecular pieces of the Alzheimer's puzzle
Researchers have uncovered a biological link between the protein whose mutation causes early-onset Alzheimer’s disease (AD) and a gene variant linked to late-onset AD. The researchers said their finding could lead to new approaches to treating AD.
Scientists Seek to Block Progression of Alzheimer’s Disease with Novel Medication that Targets the Source
(PhysOrg.com) -- Researchers at the University of California, San Diego Shiley-Marcos Alzheimer’s Research Center (ADRC) are conducting studies on an experimental medication to block nerve damage and inflammation in the brain that can lead to progressive memory loss and behavioral changes in people with Alzheimer’s disease. While current Alzheimer’s disease therapies focus on improving symptoms, this study aims to attack the root of the disease progression. Nationwide, 400 volunteers with mild to moderate Alzheimer’s disease are needed to further test this new approach.
Alzheimer's disease breakthrough
CSIRO scientists have developed a new system to screen for compounds that can inhibit one of the processes that takes place during the progression of Alzheimer’s disease.