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Data from 1,425 cognitively healthy older adults (70-89) has found that a diagnosis of chronic obstructive pulmonary disease (COPD) was associated with an 83% greater risk of developing non-amnestic mild cognitive impairment. The greatest risk was among patients who had COPD for more than five years.

A study involving 97 healthy older adults (65-89) has found that those with the “Alzheimer’s gene” (APOe4) who didn’t engage in much physical activity showed a decrease in hippocampal volume (3%) over 18 months. Those with the gene who did exercise showed no change in the size of their

An Indian study involving 648 dementia patients, of whom 391 were bilingual, has found that, overall, bilingual patients developed dementia 4.5 years later than the monolingual ones. There was no additional advantage to speaking more than two languages.

A study, involving 371 patients with mild cognitive impairment, has found that those with depressive symptoms had higher levels of amyloid-beta, particularly in the frontal cortex and the anterior and posterior cingulate gyrus (both involved in mood disorders such as depression).

A study involving 206 spousal and adult children caregivers of dementia sufferers (mostly Alzheimer’s) has found that about 84% of caregivers reported a clinically significant burden. Three factors were significant contributors to the burden:

A study involving 254 people with dementia living at home has found that 99% of people with dementia and 97% of their caregivers had one or more unmet needs, 90% of which were safety-related. More than half of the patients had inadequate meaningful daily activities at a senior center or at home, one-third still needed a dementia evaluation or diagnosis, and more than 60% needed medical care for conditions related or unrelated to their dementia.

A new U.S. study suggests that Alzheimer's disease and other dementias are markedly under-reported on death certificates and medical records. Death certificates tend to only provide an immediate cause, such as pneumonia, and don’t mention the underlying condition that provoked it.

It’s often argued that telling people that they carry genes increasing their risk of Alzheimer’s will simply upset them to no purpose. A new study challenges that idea.

11 new genetic susceptibility factors for Alzheimer’s identified

The largest international study ever conducted on Alzheimer's disease (I-GAP) has identified 11 new genetic regions that increase the risk of late-onset Alzheimer’s, plus 13 other genes yet to be validated. Genetic data came from 74,076 patients and controls from 15 countries.

Eleven genes for Alzheimer's disease have previously been identified.

Understanding a protein's role in familial Alzheimer's disease

A brain imaging study of 162 healthy babies (2-25 months) has found that those who carried the ApoE4 gene (60 of the 162) tended to have increased brain growth in areas in the

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

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.

A pilot study involving 94 older adults, of whom 18 had Alzheimer’s, 24 had

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.

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.

Comparison of the EEGs of 27 healthy older adults, 27 individuals with mild Alzheimer's and 22 individuals with moderate cases of Alzheimer’s, has found statistically significant differences across the three groups, using an algorithm that dissects brain waves of varying frequencies.

Data from two longitudinal studies of older adults (a nationally representative sample of older adults, and the Alzheimer’s Disease Neuroimaging Initiative) has found that a brief cognitive test can distinguish memory decline associated with healthy aging from more serious memory disorders, years before obvious symptoms show up.

Moreover, the data challenge the idea that memory continues to decline through old age: after excluding the cognitively impaired, there was no evidence of further memory declines after the age of 69.

Analysis of 40 spinal marrow samples, 20 of which belonged to Alzheimer’s patients, has identified six proteins in spinal fluid that can be used as markers for Alzheimer's. The analysis focused on 35 proteins that are associated with the lysosomal network — involved in cleaning and recycling beta amyloid.

Data from 848 adults of all ages has found that brain volume in the default mode network declined in both healthy and pathological aging, but the greatest decline occurred in Alzheimer’s patients and in those who progressed from mild cognitive impairment to Alzheimer’s disease.

New research supports the classification system for preclinical Alzheimer’s proposed two years ago. The classification system divides preclinical Alzheimer's into three stages:

Stage 1: Levels of amyloid beta begin to decrease in the spinal fluid. This indicates that the substance is beginning to form plaques in the brain.

Stage 2: Levels of tau protein start to increase in the spinal fluid, indicating that brain cells are beginning to die. Amyloid beta levels are still abnormal and may continue to fall.

Initial findings from an analysis of cerebrospinal fluid taken between 1995 and 2005 from 265 middle-aged healthy volunteers, of whom 75% had a close family member with Alzheimer’s disease, has found that the ratios of phosphorylated tau and amyloid-beta could predict mild cognitive impairment more than five years before symptom onset — the more tau and less amyloid-beta, the more likely

Cognitive testing for dementia has a problem in that low scores on some tests may simply reflect a person's weakness in some cognitive areas, or the presence of a relatively benign form of mild cognitive impairment (one that is not going to progress to dementia). A 2008 study found that one of every six healthy adults scored poorly on two or more of 10 tests in a brief cognitive battery. Following this up, the same researchers now show that a more holistic view might separate those who are on the path to dementia from those who are not.

A French study has predicted with 90% accuracy which patients with mild cognitive impairment would receive a clinical diagnosis of Alzheimer's disease within the following two years. The best neurological predictors were cortical thickness in two brain regions (the right

Studies linking head trauma with increased risk and earlier age of onset for Alzheimer's disease have yielded contradictory results.

A survey of 7,072 older adults in six provinces across China, with one rural and one urban community in each province, has identified 359 older adults with dementia and 328 with depression. There were only 26 participants who had doctor-diagnosed dementia reported and 26 who had doctor-diagnosed depression. Overall, 93% of dementia cases and 93% of depression were not detected.

Undetected dementia was strongly associated with low socioeconomic status such as a low educational and occupational class, and living in a rural area.

A survey of 7796 older adults (65+) living in three geographic areas in England has allowed us to compare dementia rates over time, with an identical survey having been taken between 1989 and 1994. The overall prevalence of dementia fell significantly, from 8.3% to 6.5%.

The finding provides further evidence that a cohort effect exists in dementia prevalence.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2813%2961570-6/fulltext

A large Danish study comparing two groups of nonagenarians born 10 years apart has found that not only were people born in 1915 nearly a third (32%) more likely to reach the age of 95 than those in the 1905 cohort, but members of the group born in 1915 performed significantly better on tests of cognitive ability and activities of daily living. Additionally, significantly more members of the later cohort scored maximally on the MMSE (23% vs 13% of the earlier cohort).

People with Parkinson’s disease have a six times greater risk of developing dementia than the general population. A new study points to a way of picking out those who are at risk of dementia.

A five-year study involving 525 older adults (70+) found 46 had Alzheimer’s or aMCI and a further 28 went on to develop the conditions. The blood levels of 10 specific lipids predicted with more than 90% accuracy whether an individual would go on to develop either Alzheimer’s or aMCI within 2-3 years. The researchers speculate that the lower lipid levels could be an early indication that brain cells are beginning to lose their integrity and break down.

A three-year study involving 152 adults aged 50 and older, of whom 52 had been recently diagnosed with mild cognitive impairment and 31 were diagnosed with Alzheimer's disease, has found that those with mild or no cognitive impairment who initially had amyloid-beta plaques showed greater cognitive decline than those whose brain scans were negative for plaques.

More evidence for early changes in the eye in Alzheimer’s disease comes from a study involving both rats and postmortem human retinas. Changes were found in the retinal pigment epithelial layer (which harbors the supportive cells located in the back of the eye) and in the thickness of the choroidal layer that has blood vessels providing nutrients to the retina.

The finding is consistent with growing evidence that glaucoma is a neurodegenerative disorder similar to Alzheimer’s.

Analysis of 1,821 Alzheimer’s brains has found that 11% of them actually suffered from a variant called hippocampal sparing Alzheimer’s. This subtype has been neither well recognized nor treated appropriately, but is now revealed to be relatively common.

Blocking a receptor involved in inflammation in the brains of mice with severe Alzheimer’s produced marked recovery in blood flow and vascular reactivity, a dramatic reduction in toxic amyloid-beta, and significant improvements in learning and memory.

The receptor was the bradykinin B1 receptor (B1R), and the finding confirms a role of B1R, and neuroinflammation, in the development of Alzheimer’s. It also points to a new target for therapy.

A multi-year study involving 207 healthy older adults, in which their spinal fluids were repeatedly sampled and their brains repeatedly scanned, has found that disruptions in the default mode network emerges about the same time as chemical markers of Alzheimer’s appear in the spinal fluid (decreased amyloid-beta and increased tau protein). The finding suggests not only that amyloid-beta and tau pathology affect default mode network integrity early on, but that scans of brain networks may be an equally effective and less invasive way to detect early disease.

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