Healthy older brains have not significantly reduced over time according to new research.

The belief that healthy older brains is substantially smaller than younger brains not are possibly arising from studies, people which go undetected, slowly developing brain disease was, kill cells in key areas, according to new research.

As a result, previous findings can atrophy and normal size for the older brain underestimated by the report "the prevalence of cortical gray matter atrophy may be overestimated in healthy aging brain," appears in the issue September 2009 the American Psychological Association Journal of Neuropsychology have overestimated.

The new brain study tested participants in Holland's long-term Maastricht aging study, who freely neurological problems such as dementia, Alzheimer's disease, Crohn's disease Parkinson's disease or stroke. Once participants were different from healthy, they took neuropsychological tests, including a screening test for dementia on the baseline and every three years for nine years.

The participants received in year 3, seven different parts of the brain MRI scans to measure areas and the frontal and cingulate areas of the cognitive critical cortex including memory-laden hippocampus, the areas around the hippocampus as e.g. Parahippocampal.Hippocampus plays an important role in the long-term and spatial navigation during field Parahippocampal, the hippocampus surrounds an important role in memory encoding and retrieval plays.

Dementia and Alzheimer's disease hippocampus is one of the first regions of the brain damage suffered; problems with memory and disorientation appear cingulate areas of cognitive critical cortex functions under the first Symptome.Die as an integral part of the limbic system that emotion formation and processing, learning, memory and respiratory control.

Study yields surprising results

After examining the behavioral data collected from 1994 to 2005 (with MRIs taken between 1997 and 1999 depending if people entered the study), the researchers participants divided into two groups: a group of 30 people showed significant cognitive decrease but were still dementia-free (average starting age 69.2 years) and a group of 35 cognitively healthy people stayed free of dementia (average starting age 69.1 years).

Cognitive decline was by drop of at least 30 per cent to two or more of the six core tests of the verbal learning and fluid, callback, processing speed, and complex information processing and/or drop of 3 or more points, fairs or scores of 24 or lower (raising suspicion for cognitive impairment) on the mini-mental state examination screening tool for dementia.

30 People cognitively over nine years showed a significant effect for ages in the hippocampus and Parahippocampal declined and in the frontal and cingulate Cortices while 35 cognitively healthy people nicht.Unter had the older participants the people whose understanding is deteriorating, smaller brain areas as younger Teilnehmer.Laut reflects the authors the apparent age atrophy in gray matter more likely pathological changes in the brain, the significant cognitive decline as aging itself behind.

The bottom line

As long as people remain healthy cognitive, the gray matter of areas could support of cognition don't ever verkleinert.Den according to researchers, should these findings scientists caution on conclusions of brain studies that use objective definitions and screen participants in the course of time.

View the original article here

Cell mutations to age to apoptosis lead may according to recent bear.

A study has found that mutations in the mitochondrial DNA of obesity and lack of movement-not oxidative stress before free Radikalen--may be a key factor in the aging process of the study, published in this Friday's issue of the journal Science, University of Florida finds that promote accumulation of mitochondrial mutations, the apoptosis or programmed cell death, aging drive may be a central mechanism and may regardless of version radicals free, previously thought to cause aging. This may the cellular powerhouse that converts food into energy due to the accumulation of DNA mutations in the mitochondrial DNA. Results from the study can be more effective methods to prevent aging and underline the importance of a healthy lifestyle, Christiaan Leeuwenburgh, associate professor at the Department of aging and geriatric research in the College of medicine and post said study author lead. He estimated that average maximum human life from the current 70 years on more than 100 years with exercise and a proper diet could be increased. "All therapies is intended to reduce free radical production in the mitochondria, and now looks like the non-exhaustive sense make it", he said. Breeding to recognize mice with the disabilities and repair errors in the DNA replication process discovered researchers there has been no increase in oxidative stress despite increased co-investor. However, said there was a significant increase of apoptosis, Leeuwenburgh. In mammals, uncorrected errors can cause that genetic diseases, ageing or even to death, PhD student Asimina Hiona, which was much in the biochemical analysis of free radicals and apoptosis in the study said. In mutant mice the ability was impaired, so that the cells could not repair. Finding refutes the theory of aging, indicating that increases of mitochondrial mutations increase oxidative damage, which is a cause of aging believed mitochondrial "vicious circle". "Previously believed, that you, the more free more mitochondrial mutations producing radicals you go", said Leeuwenburgh. "But this is one thing, this paper shows that this is not necessarily the case." The mice used in the study both the paper and Greg Kujoth, an Assistant Scientist were of Thomas Prolla, a professor and senior investigator bred the genetics Department at the University of Wisconsin. "Accelerated aging mice can one system links to discover, improve function in aging individuals and maybe stop or prevent that some of the diseases associated with ageing," said Prolla. The researchers discovered that on average the mutant mice so long lived one third as normal mice. Only nine months old she experienced significant loss of hair, consultation, bone mass, intestinal lining and total weight, conditions the similar to those of an aging people. Unchanged, the same mice usually 30 to 32 months life. Also, no programmed cell death between mutant and control was observed mice at the age of 3 months. Time reached mice 9 months found but significant quantities of programmed cell death in the testicles, heart, thymus and other organs. Although, the mice were considered a "model" of aging, you was a chronic inflammatory component that can cause, cardiovascular disease, Alzheimer's disease and other health problems affecting, as you age individuals. Chronic inflammation is associated with increased production of free radicals produced by other sources, such as white blood cells. "As we age we will become stiff and have pain and processes, the inflammation," said Leeuwenburgh. He added that inflammation can be prevented by an ideal body weight by caloric restriction and movement. If a healthy human lifestyle, then the stem cells therapy, nano-technology practice and special exercise and dietary interventions are even better, he said.

View the original article here