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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.

An analysis of the anatomical connectivity in the brains of 15 people with Alzheimer's disease, 68 with mild cognitive impairment and 28 healthy older individuals, has found several measures showed disease effects:

The first detailed characterization of the molecular structures of amyloid-beta fibrils that develop in the brains of those with Alzheimer's disease suggests that different molecular structures of amyloid-beta fibrils may distinguish the brains of Alzheimer's patients with different clinical histories and degrees of brain damage.

A study involving mice lacking a master clock gene called Bmal1 has found that as the mice aged, their brains showed patterns of damage similar to those seen in Alzheimer's disease and other neurodegenerative disorders. Many of the injuries seemed to be caused by free radicals.

A new study involving 96 older adults initially free of dementia at the time of enrollment, of whom 12 subsequently developed mild Alzheimer’s, has clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads.

Analysis of 5715 cases from the National Alzheimer's Coordinating Center (NACC) database has found that nearly 80% of more than 4600 Alzheimer's disease patients showed some degree of vascular pathology, compared with 67% of the controls, and 66% in the Parkinson's group. The link was especially strong for younger patients with Alzheimer’s.

The jugular venous reflux (JVR) occurs when the pressure gradient reverses the direction of blood flow in the veins, causing blood to leak backwards into the brain. A small pilot study has found an association between JVR and

The

Following on from the evidence that Alzheimer’s brains show higher levels of metals such as iron, copper, and zinc, a mouse study has found that amyloid plaques in Alzheimer’s-like brains with significant neurodegeneration have about 25% more copper than those with little neurodegeneration. This is consistent with a human study showing very high levels of copper in Alzheimer’s plaques.

Iron, though doubled in Alzheimer’s brains compared to controls, was not significantly different as a function of neurodegeneration, and zinc showed very little difference.

An Italian study has found that a significant percentage of Alzheimer’s patients suffer from Obstructive Sleep Apnea Syndrome. This respiratory disorder, which causes people to temporarily stop breathing during their sleep, affects cerebral blood flow, promoting cognitive decline. The finding adds to evidence that detecting and treating OSA early is important for preventing cognitive decline and dementia.

http://www.eurekalert.org/pub_releases/2013-10/ip-apn100813.php

Data from 70 older adults (average age 76) in the Baltimore Longitudinal Study of Aging has found that those who reported poorer sleep (shorter sleep duration and lower sleep quality) showed a greater buildup of amyloid-beta plaques.

http://www.eurekalert.org/pub_releases/2013-10/tjnj-lsa101813.php

A new discovery helps explain why the “Alzheimer’s gene” ApoE4 is such a risk factor. It appears that ApoE4 causes a dramatic reduction in SirT1, an "anti-aging protein" that is targeted by resveratrol (present in red wine).

Analyses of cerebrospinal fluid from 15 patients with Alzheimer's disease, 20 patients with mild cognitive impairment, and 21 control subjects, plus brain tissue from some of them, has found that those with Alzheimer’s had lower levels of a particular molecule involved in resolving inflammation. These ‘specialized pro-resolving mediators’ regulate the tidying up of the damage done by inflammation and the release of growth factors that stimulate tissue repair.

Tau protein stabilizes structures that transport supplies from the center of the cell to the extremities, but sometimes some tau is not bound to these microtubules and instead clumps together into

A study involving genetically engineered fruit flies adds to our understanding of why sleep and bioclock disruptions are common in those with Alzheimer's disease. People with Alzheimer's often have poor biological rhythms — periods of sleep become shorter and more fragmented, resulting in periods of wakefulness at night and snoozing during the day. It has been thought that Alzheimer’s destroys the biological clock, but this new study indicates that the clock is still working — however, it’s being ignored by other parts of the brain.

A new study shows that a combination of inflammation and hypoxia activates microglia in a way that persistently weakens the connection between neurons, contributing to brain damage in conditions such as stroke and Alzheimer's disease.

http://www.eurekalert.org/pub_releases/2014-03/uobc-scb031214.php

Brain scans of 10 persons with Down syndrome but no dementia, 10 persons with Down syndrome and dementia, and 10 healthy controls, have revealed a linear correlation between cognitive ability and compromised

A new function has been found for the

New research helps explain the role of amyloid-beta plaques in the development of Alzheimer's, by finding that the prion protein known to bind strongly to small aggregates of amyloid-beta peptides, also attaches to large fibrillar clumps of amyloid-beta.

Creating amyloid-beta requires the convergence of a protein called

A Finnish study involving moderately obese adult patients with mild obstructive sleep apnea (OSA) has found that even a modest weight loss (5%) can improve OSA, if occurring in the early stages of OSA.

http://www.eurekalert.org/pub_releases/2014-02/uoef-emw021114.php

Data from a survey of 20,000 people across the UK has found that people who cycle, walk, or take public transport to work had a lower risk of being overweight than those who drove or took a taxi. People who walked to work were 40% less likely to have diabetes than those who drove and 17% less likely to have high blood pressure. Cyclists were around half as likely to have diabetes as drivers.

http://www.eurekalert.org/pub_releases/2013-08/icl-wtw080513.php

A Swedish study of some 4,000 60-year-olds has found that regular “non-exercise” physical activity such as gardening or DIY significantly reduced risk of heart attack or stroke, with those who were most active on a daily basis having a 27% lower risk of a heart attack or stroke and a 30% reduced risk of death from all causes. This was so regardless of how much regular formal exercise was taken.

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