动物实验 z-bo 2020-09-05 422

　　With age, memory function is usually affected. Understanding and preventing this potential situation is a top priority for many scientists. Now, the recently published research goes further than ours. A recent study investigated hippocampal proteins that may be associated with age-related cognitive decline. As we age, certain aspects of cognitive ability decline. This does not apply to everyone, and not everyone is equally affected, but it usually results in insufficient memory. As our life expectancy increases, our worries about mental aging also increase. So far, researchers have identified hundreds of genes related to the aging process. For example, in 1988, scientists discovered that certain genetic mutations in nematodes (specific worms) extended the maximum life span by 110%. Since then, more than 800 individual genes that affect the lifespan of nematodes have been identified, and these genes are also abundant in other species. Although the genes related to aging are slowly developing, understanding their role and how they affect them is another challenge.

　　Recently, Philip Landfield (Philip Landfield), John Gantt (John Gantt), Eric Bralock (Eric Bralock) and others have conducted a number of studies at the University of Lexington, Kentucky. They wanted to understand the role of certain proteins in memory loss in mice and how they affect age-related genetic changes. A protein called FK506 binding protein 12.6/1b (FKBP1b) can regulate the calcium homeostasis of hippocampal neurons, which are areas of the brain related to spatial memory that can convert short-term memory into long-term memory. When researchers look for ways to change brain aging, they always find that the physiological role of calcium has changed. A previous study by the same group found that blocking FKBP1b can prevent the use of calcium in the hippocampus. The authors also found that FKBP1b gene expression is down-regulated in the hippocampus of aging rats and patients with early Alzheimer's disease. \r\nDetails of FKBP1b\nThey want to study the latest research on how FKBP1b processing affects memory and age-related genetic changes in old rats. .. When injected into rats with viral vectors expressing FKBP1b, they increased total protein expression. The injection is 13 months (called long-term) or 19 months (called short-term) before the onset of cognitive decline.

　　Their findings were announced in the Journal of Neuroscience this week. Long-term and short-term treatment can improve the behavior of mice in the water maze. FKBP1b can prevent long-term cognitive decline in rats and reverse the short-term cognitive decline in rats. Compared with untreated rats of the same age,\ntreated rats completed better memory tasks, and their scores were more consistent with untreated young rats. \r\nNext, the researchers conducted a transcription analysis. They identified 2,342 genes that are differentially expressed in young and old animals. Treatment with FKBP1b can restore the activity of 876 of these age-affected genes. In fact, its level is similar to that of untreated puppies. Modified genes may be involved in the regulation of hippocampal structure and function, and "represent a new genome network" that is damaged with age. The author concludes: "His genomic evidence strongly supports the hypothesis that FKBP1b is the key to neuronal homeostasis. This functional regulation [calcium], structural integrity and the latest findings of these studies. Provide further evidence that FKBP1b Participated in cognitive aging, especially memory loss.\n\nage With age, memory function is usually affected, so understanding and preventing this potential situation is a top priority for many scientists. A recent study further investigated Hippocampal protein, which may be related to age-related cognitive decline. This reduces some aspects of.. Not applicable to everyone, and not everyone is affected equally, but usually leads to insufficient memory

　　As time goes by, there are more and more worries about mental aging. So far, researchers have identified hundreds of genes related to the aging process. For example, in 1988, scientists discovered nematodes (it has been found that certain genetic mutations in worms extend the maximum life span by 110%, because by then, More than 800 individual genes that affect the lifespan of nematodes have been identified, and these genes have also been identified in other species. The genes associated with aging are slowly developing, but understanding their role and how they affect them is another challenge. Kentucky University, Lexington, Philip Landfield, John Gunter, Eric Bralock and others have studied the role of certain proteins in memory loss in mice and their genetic age-related characteristics. I think Learn how it affects changes: A protein called FK506 binding protein 12.6/1b (FKBP1b) was found in hippocampal neurons, which is related to spatial memory and can convert short-term memory into long-term memory. When researchers look for changes When the brain is aging, they always find that the physiological role of calcium has changed. Early studies in the same group have shown that FKBP1b is blocked. It has been found that lock-in prevents the use of calcium in the hippocampus. The authors also found that FKBP1b gene expression increases in aging. It is down-regulated in the hippocampus of rats and early Alzheimer's disease patients.

　　FKBP1b's detailed information

　　They want to study how FKBP1b treatment affects the memory and age-related genetic changes in old rats. When injected into rats with viral vectors expressing FKBP1b, they increased total protein expression. The injection is 13 months (called long-term) or 19 months (called short-term) before the onset of cognitive decline. Their findings were announced in the Journal of Neuroscience this week. Long-term and short-term treatment can improve the behavior of mice in the water maze. FKBP1b can prevent long-term cognitive decline in rats and reverse the short-term cognitive decline in rats. Compared with untreated rats of the same age, treated rats completed better memory tasks, and their scores were more consistent with untreated young rats.

　　Next, the researchers performed transcription analysis. They identified 2,342 genes that are differentially expressed in young and old animals. Treatment with FKBP1b can restore the activity of 876 of these age-affected genes. In fact, its level is similar to that of untreated puppies. The modified genes may be involved in the regulation of hippocampal structure and function, and "represent a new genome network that is damaged with age." The author's conclusion is:

　　"His genomic evidence strongly supports the hypothesis that FKBP1b is the key to neuronal homeostasis. Functional regulation [calcium], structural integrity, these latest findings indicate that FKBP1b we provide further evidence that we know that aging, especially memory loss ,play an important role.