seniors

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 white matter changes in the brains of patients with Alzheimer’s disease and those with mild cognitive impairment. This suggests that cerebral venous outflow impairment might play a role in the development of white matter changes in those with Alzheimer’s.

The hippocampus is damaged early in Alzheimer’s, while the thalamus is generally unaffected until the late stages. Brain imaging of the hippocampus and the thalamus in 31 patients with Alzheimer's and 68 healthy controls has revealed increased levels of iron in the hippocampus of those with Alzheimer’s, but not in the thalamus. Moreover, this increased iron was associated with tissue damage in patients with Alzheimer's but not in the healthy older individuals.

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). This reduction in SirT1 was associated with a change in the way the amyloid precursor protein (APP) was processed. Moreover, there was evidence that ‘bad’ tau and amyloid-beta could be prevented by increasing SirT1.

http://www.eurekalert.org/pub_releases/2013-10/bifa-mar101613.php

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. Lower levels of these molecules also correlated with a lower degree of cognitive function.

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 neurofibrillary tangles — one of the hallmarks of Alzheimer's disease, and also linked to other neurodegenerative disorders. A new study supports the theory that ‘bad’ tau travels to different brain regions via the synapses — that is, it’s secreted with the signals passing between neurons.

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