Positive Technology Journal

Via Medgadget

Georgia Tech/Emory researchers are testing how to use dopamine to design polymer that could help damaged nerves reconnect. Their discovery might lead to the development of new therapies for a range of central and peripheral nervous system disorders:

The discovery is the first step toward the eventual goal of implanting the new polymer into patients suffering from neurological disorders, such as Alzheimer's, Parkinson's or epilepsy, to help repair damaged nerves. The findings were published online the week of Oct. 30 in the Proceedings of the National Academy of Sciences (PNAS).

"We showed that you could use a neurotransmitter as a building block of a polymer," said Wang. "Once integrated into the polymer, the transmitter can still elicit a specific response from nerve tissues."

The "designer" polymer was recognized by the neurons when used on a small piece of nerve tissue and stimulated extensive neural growth. The implanted polymer didn't cause any tissue scarring or nerve degeneration, allowing the nerve to grow in a hostile environment post injury.

When ready for clinical use, the polymer would be implanted at the damaged site to promote nerve regeneration. As the nerve tissue reforms, the polymer degrades.

Wang's team found that dopamine's structure, which contains two hydroxyl groups, is vital for the material's neuroactivity. Removing even one group caused a complete loss of the biological activity. They also determined that dopamine was more effective at differentiating nerve cells than the two most popular materials for culturing nerves -- polylysine and laminin. This ability means that the material with dopamine may have a better chance to successfully repair damaged nerves.

The success of dopamine has encouraged the team to set its sights on other neurotransmitters.

"Dopamine was a good starting point, but we are looking into other neurotransmitters as well," Wang said.

The team's next step is to verify findings that the material stimulates the reformation of synapses in addition to regrowth.

Via Medline

Geriatricians from Saint Louis University have developed a new test for diagnosing dementia - the Saint Louis University Mental Status Examination (SLUMS) - which appears to be more effective than the widely-used Mini Mental Status Examination (MMSE). 

The study has been published in the current issue of the American Journal of Geriatric Psychiatry (14:900-910, November 2006)

From the news release

"This early detection of mild neurocognitive disorder by the SLUMS offers the opportunity for the clinicians to begin early treatment as it becomes available," says Syed Tariq, M.D., lead author and associate professor of geriatric medicine at Saint Louis University.

John Morley, M.D., director of the division of geriatric medicine at Saint Louis University, created the SLUMS to screen more educated patients and to detect early cognitive problems.

"There are potential treatments available and they slow down the progression of the disease," says Morley, who is a coinvestigator. "The earlier you treat, the better people seem to do. But families go through denial and sometimes miss diagnosing dementia until its symptoms are no longer mild."

The researchers found the new screening tool developed by SLU detects early cognitive problems missed by the MMSE.

"The Mini Mental Status Examination has limitations, especially with regard to its use in more educated patients and as a screen for mild neurocognitive disorder," Tariq says.

It takes a clinician about seven minutes to administer the SLUMS, which supplements the Mini Mental Status Examination by asking patients to perform tasks such as doing simple math computations, naming animals, recalling facts and drawing the hands on a clock.

Via The Neurophilosopher 

Boosting slow oscillations during sleep potentiates memory

Nature advance online publication 5 November 2006

Authors: Lisa Marshall, Halla Helgadóttir, Matthias Mölle and Jan Born

There is compelling evidence that sleep contributes to the long-term consolidation of new memories. This function of sleep has been linked to slow (<1 Hz) potential oscillations, which predominantly arise from the prefrontal neocortex and characterize slow wave sleep. However, oscillations in brain potentials are commonly considered to be mere epiphenomena that reflect synchronized activity arising from neuronal networks, which links the membrane and synaptic processes of these neurons in time. Whether brain potentials and their extracellular equivalent have any physiological meaning per se is unclear, but can easily be investigated by inducing the extracellular oscillating potential fields of interest. Here we show that inducing slow oscillation-like potential fields by transcranial application of oscillating potentials (0.75 Hz) during early nocturnal non-rapid-eye-movement sleep, that is, a period of emerging slow wave sleep, enhances the retention of hippocampus-dependent declarative memories in healthy humans. The slowly oscillating potential stimulation induced an immediate increase in slow wave sleep, endogenous cortical slow oscillations and slow spindle activity in the frontal cortex. Brain stimulation with oscillations at 5 Hz—another frequency band that normally predominates during rapid-eye-movement sleep—decreased slow oscillations and left declarative memory unchanged. Our findings indicate that endogenous slow potential oscillations have a causal role in the sleep-associated consolidation of memory, and that this role is enhanced by field effects in cortical extracellular space.