Health & age-related problems

Drug derived from curcumin may help treat stroke

March, 2011

More evidence for the value of the curry spice curcumin comes from animal studies indicating a curcumin-derived drug may help treat stroke.

A new molecular compound derived from curcumin (found in turmeric) holds promise for treating brain damage caused by stroke. Turmeric has a long history of use in Ayurvedic and Chinese traditional medicine. However, curcumin has several important drawbacks as far as treating stroke is concerned — mainly because it can’t cross the blood-brain barrier. The new compound can.

In rabbit experiments, the drug was effective when administered up to an hour after stroke, which correlates with about three hours in humans. This is the same time frame for which tPA — the only drug currently approved for ischemic stroke — is currently approved.

The new drug is expected to move to human clinical trials soon.

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Paul A. Lapchak presented these findings at the American Heart Association International Stroke Conference in Los Angeles on February. 9.

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Acupressure may help treat TBI

March, 2011

A placebo-controlled study reveals a treatment for mild traumatic brain injury that sufferers can administer themselves.

A study involving 38 people suffering from mild traumatic brain injury (TBI) has found that those receiving acupressure treatments from trained experts (eight treatments over 4 weeks) scored significantly better on tests of working memory compared to those who received treatments from the same experts on places on the body that are not considered to be acupressure points.

Acupressure involves the practitioner using his fingertips to stimulate particular points on a person's body. The acupressure treatment type used in the study was Jin Shin. This treatment can be taught to family and friends of those with TBI and can even be used as a self-treatment, making it a good candidate for an adjunct treatment for TBI.

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Migraines and headaches linked to more brain lesions in older adults

March, 2011

Older adults who have a history of severe headaches are more likely to have a greater number of brain lesions, but do not show greater cognitive impairment (within the study time-frame).

Lesions of the brain microvessels include white-matter hyperintensities and the much less common silent infarcts leading to loss of white-matter tissue. White-matter hyperintensities are common in the elderly, and are generally regarded as ‘normal’ (although a recent study suggested we should be less blasé about them — that ‘normal’ age-related cognitive decline reflects the presence of these small lesions). However, the degree of white-matter lesions is related to the severity of decline (including increasing the risk of Alzheimer’s), and those with hypertension or diabetes are more likely to have a high number of them.

A new study has investigated the theory that migraines might also lead to a higher number of white-matter hyperintensities. The ten-year French population study involved 780 older adults (65+; mean age 69). A fifth of the participants (21%) reported a history of severe headaches, of which 71% had migraines.

Those with severe headaches were twice as likely to have a high quantity of white-matter hyperintensities as those without headaches. However, there was no difference in cognitive performance between the groups. Those who suffered from migraines with aura (2% of the total), also showed an increased number of silent cerebral infarcts — a finding consistent with other research showing that people suffering from migraine with aura have an increased risk of cerebral infarction (or strokes). But again, no cognitive decline was observed.

The researchers make much of their failure to find cognitive impairment, but I would note that, nevertheless, the increased number of brain lesions does suggest that, further down the track, there is likely to be an effect on cognitive performance. Still, headache sufferers can take comfort in the findings, which indicate the effect is not so great that it shows up in this decade-long study.

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Memory problems may be more about interference than forgetting

February, 2011

An animal study points to confusion between memories being central to amnesia, rather than a failure to recall.

We have thought of memory problems principally in terms of forgetting, but using a new experimental method with amnesic animals has revealed that confusion between memories, rather than loss of memory, may be more important.

While previous research has found that amnesic animals couldn't distinguish between a new and an old object, the new method allows responses to new and old objects to be measured separately. Control animals, shown an object and then shown either the same or another object an hour later, spent more time (as expected) with the new object. However, amnesic animals spent less time with the new object, indicating they had some (false) memory of it.

The researchers concluded that the memory problems were the result of the brain's inability to register complete memories of the objects, and that the remaining, less detailed memories were more easily confused. In other words, it’s about poor encoding, not poor retrieval.

Excitingly, when the amnesic animals were put in a dark, quiet space before the memory test, they performed perfectly on the test.

The finding not only points to a new approach for helping those with memory problems (for example, emphasizing differentiating details), but also demonstrates how detrimental interference from other things can be when we are trying to remember something — an issue of particular relevance in modern information-rich environments. The extent to which these findings apply to other memory problems, such as dementia, remains to be seen.

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Predicting memory loss in healthy older adults

February, 2011

Having the ‘Alzheimer’s gene’ and showing reduced brain activity during a mental task combined to correctly predict future cognitive decline in 80% of healthy elders.

In a study in which 78 healthy elders were given 5 different tests and then tested for cognitive performance 18 months later, two tests combined to correctly predict nearly 80% of those who developed significant cognitive decline. These tests were a blood test to identify presence of the ‘Alzheimer’s gene’ (APOE4), and a 5-minute fMRI imaging scan showing brain activity during mental tasks.

The gene test in itself correctly classified 61.5% of participants (aged 65-88; mean age 73), showing what a strong risk factor this is, but when taken with activity on the fMRI test, the two together correctly classified 78.9% of participants. Age, years of education, gender and family history of dementia were not accurate predictors of future cognitive decline. A smaller hippocampus was also associated with a greater risk of cognitive decline.

These two tests are readily available and not time-consuming, and may be useful in identifying those at risk of MCI and dementia.

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Woodard, J.L.  et al. 2010. Prediction of Cognitive Decline in Healthy Older Adults using fMRI. Journal of Alzheimer’s Disease, 21 (3), 871-885.

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Compound derived from curry spice helps in stroke and TBI

January, 2011

Two new animal studies offer hope for a drug treatment for traumatic brain injury and stroke.

Following indications that the curry spice curcumin (the active ingredient in turmeric) may help protect brain cells from damage, two new studies have been testing a compound called CNB-001, derived from curcumin.

The first (rabbit) study found that CNB-001 is at least as effective as the only existing drug used to treat stroke (TPA), without the unwanted side-effect of reducing clotting in the blood vessels of the brain.

The second study found that CNB-001 dramatically reversed the behavioral deficits in both locomotion and memory in brain-injured rats. As with stroke, CNB-001 was again found to maintain the critical signaling pathways required for nerve cell survival, as well as the connections between nerve cells that are lost with the injury.

At present, there is no treatment for TBI, and only one FDA-approved drug for ischemic stroke

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Cognitive recovery after brain damage more complex than realized

January, 2011

Two new studies show us that recovery after brain damage is not as simple as one region ‘taking over’ for another, and that some regions are more easily helped than others.

When stroke or brain injury damages a part of the brain controlling movement or sensation or language, other parts of the brain can learn to compensate for this damage. It’s been thought that this is a case of one region taking over the lost function. Two new studies show us the story is not so simple, and help us understand the limits of this plasticity.

In the first study, six stroke patients who have lost partial function in their prefrontal cortex, and six controls, were briefly shown a series of pictures to test the ability to remember images for a brief time (visual working memory) while electrodes recorded their EEGs. When the images were shown to the eye connected to the damaged hemisphere, the intact prefrontal cortex (that is, the one not in the hemisphere directly receiving that visual input) responded within 300 to 600 milliseconds.

Visual working memory involves a network of brain regions, of which the prefrontal cortex is one important element, and the basal ganglia, deep within the brain, are another. In the second study, the researchers extended the experiment to patients with damage not only to the prefrontal cortex, but also to the basal ganglia. Those with basal ganglia damage had problems with visual working memory no matter which part of the visual field was shown the image.

In other words, basal ganglia lesions caused a more broad network deficit, while prefrontal cortex lesions resulted in a more limited, and recoverable, deficit. The findings help us understand the different roles these brain regions play in attention, and emphasize how memory and attention are held in networks. They also show us that the plasticity compensating for brain damage is more dynamic and flexible than we realized, with intact regions stepping in on a case by case basis, very quickly, but only when the usual region fails.

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What happens after traumatic brain injury occurs?

December, 2010

Findings from a rat study show how TBI can begin a process that continues to deform the brain long after the original injury.

A rat study using powerful imaging techniques has revealed how an injured brain continues to change long after the original trauma. Widespread decreases in brain functioning over a period of months were seen in specific brain regions, in particular the hippocampus, amygdala, and ipsilateral cortex, even when these were remote from the site of direct trauma and unaccompanied by signs of injury.

The findings indicate that there is a time window during which intervention could reduce these processes and protect against some of the disabling consequences of TBI.

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More evidence for the cognitive benefit of treating sleep apnea

December, 2010

Another study has come out showing the benefits of CPAP treatment for cognitive impairment caused by obstructive sleep apnea.

Comparison of 17 people with severe obstructive sleep apnea (OSA) with 15 age-matched controls has revealed that those with OSA had reduced gray matter in several brain regions, most particularly in the left parahippocampal gyrus and the left posterior parietal cortex, as well as the entorhinal cortex and the right superior frontal gyrus. These areas were associated with deficits in abstract reasoning and executive function. Deficits in the left posterior parietal cortex were also associated with daytime sleepiness.

Happily, however, three months of treatment with continuous positive airway pressure (CPAP), produced a significant increase in gray matter in these regions, which was associated with significant improvement in cognitive function. The researchers suggest that the hippocampus, being especially sensitive to hypoxia and innervation of small vessels, is the region most strongly and quickly affected by hypoxic episodes.

The findings point to the importance of diagnosing and treating OSA.

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New brief tool to screen for cognitive impairment in elderly patients

December, 2010

A 2-minute questionnaire does an excellent job of indicating older adults with cognitive impairment.

A simple new cognitive assessment tool with only 16 items appears potentially useful for identifying problems in thinking, learning and memory among older adults. The Sweet 16 scale is scored from zero to 16 (with 16 representing the best score) and includes questions that address orientation (identification of person, place, time and situation), registration, digit spans (tests of verbal memory) and recall. The test requires no props (not even pencil and paper) and is easy to administer with a minimum of training. It only takes an average of 2 minutes to complete.

A score of 14 or less correctly identified 80% of those with cognitive impairment (as identified by the Informant Questionnaire on Cognitive Decline in the Elderly) and correctly identified 70% of those who did not have cognitive impairment. In comparison, the standard MMSE correctly identified 64% of those with cognitive impairment and 86% of those who were not impaired. In other words, the Sweet 16 missed diagnosing 20% of those who were (according to this other questionnaire) impaired and incorrectly diagnosed as impaired 30% of those who were not impaired, while the MMSE missed 36% of those who were impaired but only incorrectly diagnosed as impaired 14% of those not impaired.

Thus, the Sweet 16 seems to be a great ‘first cut’, since its bias is towards over-diagnosing impairment. It should also be remembered that the IQCDE is not the gold standard for cognitive impairment; its role here is to provide a basis for comparison between the new test and the more complex MMSE. In comparison with a clinician’s diagnosis, Sweet 16 scores of 14 or less occurred in 99% of patients diagnosed by a clinician to have cognitive impairment and 28% of those without such a diagnosis.

The great benefit of the new test is of course its speed and simplicity, and it seems to offer great promise as an initial screening tool. Another benefit is that it supposedly is unaffected by the patient’s education, unlike the MMSE. The tool is open access.

The Sweet 16 was developed using information from 774 patients who completed the MMSE, and then validated using a different group of 709 older adults.

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