October 28, 2014
In the search for the causes of Alzheimer’s disease (AD), most researchers have agreed that an abnormal level of beta-amyloid, protein plaques in the brain that disrupt neuronal communications, will lead eventually to decreased memory and thinking abilities in otherwise healthy adults, which themselves are the harbinger of ultimate progression to dementia. While it was assumed that this slow descent to mild cognitive impairment and ultimately AD was inevitable, new research released this month indicates that there may be certain genetic combinations that could slow this decline.
Over time, the accumulation of beta-amyloid kills enough cells to eventually cause severe shrinkage in brain capacity and function for
Flagship Study of Ageing (AIBL) study, and results from other groups such as ADNI, Harvard Aging Brain Study and the Mayo Clinic Olmstead County Study had shown convincingly that cognitively normal older adults with abnormally high levels of amyloid showed a reliable and relentless decline in memory and thinking abilities.”
“This decline continues until, ultimately, an individual’s memory and thinking abilities reach levels that are sufficiently low enough to warrant classification of mild cognitive impairment (MCI) due to AD. In fact, the evidence for this early decline is now considered strong enough to have warranted commencement of secondary prevention trials, where cognitively normal older adults are treated with anti-amyloid drugs.”
However, Dr. Lim and her colleagues has also been looking at the extent to which other factors influence the effect of amyloid on memory decline, in particular they have focused on the effects of two specific gene variants, the apolipoprotein E (APOE) and the brain-derived neurotrophic factor (BDNF) Va166Met, on the progression path of AD. BDNF, a secreted protein encoded by the gene, has been labeled by some as “Miracle-Gro” for the brain, strengthening existing neurons and helping new neuron cells grow.
While having the ApoE4 variant has been linked to increased risk of AD, the combination with the BDNF gene and its variants had not been investigated. Dr. Lim and a team of researchers checked for these gene variants and the levels of beta-amyloid in 333 healthy adult volunteers enrolled in the AIBL study. The participants also underwent neuropsychological testing at baseline, then at 18, 36, and 54 months. Using the Cogstate Brief Battery, a score combining the results of episodic memory, executive function, language, and attention tests was used to measure any cognitive decline in the population