February 10, 2009

Mediterranean Diet and Mild Cognitive Impairment

archneuro.jpgA observational study published this month in the Archives of Neurology evaluated 1393 cognitively normal participants found that mild cognitive impairment and its progression to Alzheimer's disease (AD) were less common in older New Yorkers adhering to the so-called Mediterranean diet

The study was a multiethnic community study which investigated the association between adherence to the Mediterranean Diet (MeDi) and the incidence of MCI as well as the progression from MCI to AD. All of the models were adjusted for cohort, age, sex, ethnicity, education, APOE genotype, caloric intake, body mass index, and duration between baseline dietary assessment and baseline diagnosis.

Among those who stuck most closely to the diet, the risk of developing mild cognitive impairment was reduced 28% relative to those with the poorest adherence. And those with mild cognitive impairment at study baseline were at 48% less risk of receiving a diagnosis of Alzheimer's disease over a mean 4.3-year period if they had good adherence to the diet, the researchers found.

The authors notes that the reductions were modest and the underlying mechanisms remain unclear. Nevertheless, they concluded that, "higher adherence to the MeDi is associated with a trend for reduced risk of developing MCI and with reduced risk of MCI conversion to AD."

The Mediterranean diet is characterized by a predominance of fish, legumes, fruits, vegetables, cereals, unsaturated fats, and regular moderate alcohol consumption.

Sources:
Archives of Neurology
MedPageToday

Posted by rsk at 08:51 AM

February 02, 2009

Brain's Single Cell Memory Buffer Revealed

neuron.jpgNew research published in the February issue of the journal Nature Neuroscience found that an individual nerve cell in the prefrontal cortical (PFC) area can hold traces of memories on its own for as long as a minute, possibly even longer. Reseachers from the Department of Psychiatry at the University of Texas Southwestern Medical Center studying mice, found that rapid-fire inputs less than a second long initiate a cellular memory process in single cells lasting as long as minute, a process called metabotropic glutamate transmission. This transmission in the most highly evolved brain region holds moment-to-moment information.

This is the first study to identify the specific signal that establishes nonpermanent cellular memory and reveals how the brain holds temporary information. According to the authors, "it has implications for addiction, attention disorders and stress-related memory loss." Researchers have known that permanent memories are stored when the excitatory amino acid glutamate activates ion channels on nerve cells in the brain to reorganize and strengthen the cells' connections with one another. But this process takes minutes to hours to turn on and off and is too slow to buffer, or temporarily hold, rapidly incoming information.

The researchers identified in mice a specific metabotropic glutamate receptor (mGluR5) that, when turned on, starts a signaling cascade using calcium to hold a memory trace. This fast, short-term memory process happens inside individual cells; with long-term memory, additional proteins cause slow reorganization between cells in a network to establish a permanent memory.

Researchers examined brain cells from mice using nanoscale electrodes to measure the memory formation process. To further understand how this short-term memory process relates to addiction, researchers applied dopamine to the memory buffer nerve cells. Dopamine is normally needed at an optimal level for an individual to focus attention and engage in fast decision-making memory, but drugs of abuse overload the brain with a surge of dopamine. In the study, researchers found that an experimental drug that activates a specific type of dopamine receptor "focused" the nerve cells, making the memory trace less susceptible to distraction.

When researchers employed an animal model of drug addiction using cocaine, they also found that repeated exposure to addictive levels of cocaine reduced memory trace activation in the memory buffer cells. When researchers then activated dopamine signaling in the "addicted" animals, essentially adding more dopamine to their systems, no focusing effect was observed.

Researchers next plan to identify the ion channel responsible for holding and regenerating a memory trace. Their goal is to develop new pharmacological and genetic tools that will allow them to manipulate and possibly expand decision-making memory capacity.

The study was funded by the National Institute on Drug Abuse; National Alliance for Research on Schizophrenia and Depression; the Alexander S. Onassis Public Benefit Foundation; and the Department of Veterans Affairs.

Sources:

Abstract
Nature Neuroscience 12, 190 - 199

How memories form, fade, and persist over time
CNN

Posted by rsk at 10:43 AM