Research

A gene linked to Alzheimer's has been linked to brain changes in childhood. This gene, SORL1, has two connections to Alzheimer’s: it carries the code for the sortilin-like receptor, which is involved in recycling some molecules before they develop into amyloid-beta; it is also involved in lipid metabolism, putting it at the heart of the vascular risk pathway.

Analysis of data from 237 patients with mild cognitive impairment (mean age 79.9) has found that, compared to those carrying the ‘normal’ ApoE3 gene (the most common variant of the ApoE gene), the ApoE4 carriers showed markedly greater rates of shrinkage in 13 of 15 brain regions thought to be key components of the brain networks disrupted in Alzheimer’s.

http://www.eurekalert.org/pub_releases/2014-01/rson-gva010714.php

Two studies indicate that young people carrying the “Alzheimer’s gene” (ApoE4) do not have the pathological changes found later in life. The first study, involving 1412 adolescents, found no differences in hippocampal volume or asymmetry as a function of gene status. The second study, involving 173 young adults (average age, 28 ± 7.6 years), found no difference in plasma concentrations of amyloid-beta peptides.

http://www.eurekalert.org/pub_releases/2014-04/ip-neo040614.php

Analysis of data from more than 8,000 people, most of them older than 60, has revealed that, among the 5,000 people initially tested cognitively normal, carrying one copy of the “Alzheimer’s gene” (ApoE4) only slightly increased men’s risk of developing MCI or Alzheimer’s — but nearly doubled women’s risk (healthy men with APOE4 were 27% more likely to develop MCI or Alzheimer’s compared to those without the gene, while female carriers had an 81% greater risk).

Analysis of 700 subjects from the Alzheimer's Disease Neuroimaging Initiative has revealed a genetic mutation (rs4728029) that’s associated with people who develop Alzheimer’s pathology but don’t show clinical symptoms in their lifetime. The gene appears to be related to an inflammatory response in the presence of phosphorylated tau. In other words, some people’s brains react to phosphorylated tau with a ‘bad’ inflammatory response, while others don’t.

Analysis of brain scans and cognitive scores of 64 older adults from the NIA's Baltimore Longitudinal Study of Aging (average age 76) has found that, between the most cognitively stable and the most declining (over a 12-year period), there was no significant difference in the total amount of amyloid in the brain, but there was a significant difference in the location of amyloid accumulation. The stable group showed relatively early accumulation in the frontal lobes, while the declining group showed it in the temporal lobes.

A pilot study involving 94 older adults, of whom 18 had Alzheimer’s, 24 had MCI, 26 other dementias, and 26 were healthy controls, has found those with Alzheimer’s were significantly less able to detect the smell of peanut butter. Peanut butter was chosen because of its purity and accessibility (not because there's something special about its smell!).

A Finnish project (ALSOVA) has been following 240 patient-caregiver pairs, where the patient had very mild or mild Alzheimer's disease at the beginning of the study and had a family caregiver. A three-year follow-up of 115 patients has found that those diagnosed and treated very early were able to manage their everyday activities longer and suffered from less psychological and behavioral symptoms, compared to those diagnosed later.

Data from 6257 older adults (aged 55-90) evaluated from 2005-2012 has revealed that concerns about memory should be taken seriously, with subjective complaints associated with a doubled risk of developing mild cognitive impairment or dementia, and subjective complaints supported by a loved one being associated with a fourfold risk. Complaints by a loved one alone were also associated with a doubled risk. Among those with MCI, subjective complaints supported by a loved one were associated with a threefold risk of converting to dementia.

Analysis of mitochondrial DNA (mtDNA) in the cerebrospinal fluid has found that both symptomatic Alzheimer’s patients and asymptomatic patients at risk of Alzheimer’s showed a significant decrease in levels of circulating cell-free mtDNA in the CSF. Patients with frontotemporal dementia did not display this.