Damaged Kidney Function may Cause Cognitive Decline in Elderly

Impaired kidney function may lead to cognitive decline in old age, according to a new study.

Conducted by researchers at Rush University Medical Center, the study found that poor kidney function was linked specifically with cognition related to memory functions.

Damage to one of these functions, episodic memory, which retrieves memories of time, place, associated emotions and other contextual knowledge, is often the earliest sign of Alzheimer's disease.

"Given the dearth of modifiable risk factors for age-related cognitive decline, these results have important public health implications. Further work to understand the link between kidney function and the brain may provide new strategies for preventing memory loss in elders," said Dr. Aron Buchman, a neuroscientist in the Rush Alzheimer's Disease Center.

He said that the findings show that there are common disease processes that affect both the brain and the kidneys in the elderly.

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Buchman also hypothesized that underlying vascular problems, such as diabetes and hypertension, may account for the association between kidney problems and cognitive decline.

The study analysed data for 886 older adults who participated in the Rush Memory and Aging Project, a group of community-dwelling seniors with a mean age of 81, all of them initially free of dementia.

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The participants were examined annually for up to six years to track changes in cognition over time.

The researchers ruled out the influence of factors like aging and medications, which can affect cognition.

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They found that poor kidney function, assessed at the beginning of the study, was linked with a more rapid rate of decline in cognition over the next several years - not in visuospatial ability or perceptual speed, but in three specific areas: episodic, semantic and working memory.

Buchman said that the rate of decline in cognition was equivalent to that of a person seven years older at baseline.

The study has been published in the journal Neurology. (ANI)

Obesity alone does not cause knee osteoarthritis |Sci-tech[Washington{Washington, Sep 29 (ANI): In a study on mice, Duke University researchers have found that obesity alone cannot lead to osteoarthritis, a progressive musculoskeletal disorder that is characterized by loss of joint cartilage.

The researchers studied leptin-deficient mice to determine the role of obesity in developing knee osteoarthritis (OA).

In their opinion, obesity caused by a leptin deficiency would result in a higher incidence of knee OA.

Mice with a disruption of leptin signalling showed a 3-fold increase in body mass and 10-fold increase in body fat, but surprisingly did not display effects of knee OA.

The researchers compared leptin-deficient and leptin receptor-deficient female mice with wild-type mice to further understand the role this deficiency may play in increasing risk of knee OA.

At 10-12 months of age, mice were measured for body fat content and blood samples were taken to determine the level of inflammation in the animals.

Knee joints were analysed to determine bone thickness and to look for degenerative changes in the lateral femur, lateral tibia, medial femur, and medial tibia.

Though higher levels of leptin are present in obese individuals, they apparently have a resistance to the effects of the hormone where the body does not receive the signal it is full after eating.

According to Dr. Farshid Guilak and colleagues, the leptin-deficient mice showed a 10-fold increase in adiposity (body fat) but not a higher incidence of OA compared with wild-type mice.

"It was surprising that knee OA was not present given the severity of obesity in the leptin-impaired mice," said Guilak.

The study implies that leptin could be directly involved in OA because without that hormone, obesity did not influence the occurrence of OA in the mice.

Mice with loss of leptin function also had reduced bone thickness beneath the cartilage and increased tissue volume at the end of the tibia, suggesting that obesity, other obesity-dependent factors, or the absence of leptin signalling independently diminishes bone structure.

The findings of the study have been published in Arthritis and Rheumatism.

Source-ANI
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