Expression Of Mir124 And 184 Decreased Dramatically

As a human get older, many of the organs will deteriorate and lost the functions. Out of all of the organs, our brains are extremely vulnerable to the process of aging. In the article of “Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice”, the researchers leaded by Saul Villeda in University of California, San Francisco, focus on the study of physical and functional property of the hippocampus in mice. Hippocampus manages the learning and memory process. However, it is extremely sensitive to aging and shows many down regulations as the brain ages. The study had also revealed the important role of Creb, which maintain hippocampus properly functional and healthy. Two different assays were used to study the role of Creb in the cognitive function and synaptic plasticity which includes testing hippocampus-related memorizing and learning processes and measuring the dendritic spine number and synaptic plasticity.

IncRNAs are excellent candidates for therapeutics development because they have recently been identified as major regulators of gene function through gene-specific modulation of transcription and translation25-32. Several studies have shown that single lncRNAs mediate complex physiological responses26,33-40. Manipulation of these lncRNAs by knockdown has yielded control of these processes41-45. Our studies will provide temporal characterization of drug-induced changes in the expression of lncRNAs in the BLA during reconsolidation to identify novel candidates for the therapeutic manipulation of reconsolidation of METH-associated memories. If time permits during the project period, we will extend our findings related to METH-associated memories to other psychostimulants and drug classes. It is also worth noting that our studies will provide novel insights into the biological functions of lncRNAs, whose function is largely a mystery, particularly in the brain. Further, the knowledge of lncRNAs that result from our studies may be applied to other memory disorders, including post-traumatic stress disorder

Consistent with the idea of learning and the brain’s interaction with the environment, neuroplasticity is the idea that the human brain can change and grow, that it can modify itself to compensate for weak spots and expand limits (Cockrell, 2007). For example, it was once thought that neuron production slows down exponentially in adulthood, but research reveals that this is not the case. Research has found that the brains of aging cancer patients were still able to produce new neurons (Cockrell, 2007). The human brain is an extremely complex organ. Inside the average human brain, there are 200 billion neurons. These neurons allow for trillions of connections (Arrowsmith, 2013). Arrowsmith (2013) discussed Mark Rosenshwag, a neuroscientist who conducted an experiment with rats. Rosenswag placed the rats in a stimulating environment and found that rats were better learners because of the stimulation. More importantly, he noted that the brains of the rats being studied changed

It is full of comprehensive and engaging style; well reference and scientifically proven, summarizes the current revolution in neuroscience and neuroplasticity, and closes the gap that the old age or matured brain, which is unchangeable is changeable and malleable (plastic); extending it functions from one region to the other. Doidge engaging style of writing, scientific proves, and academic tone help to make the book persuasive.

Synaptic plasticity refers to a process through which the brain undergoes neural changes due to alterations in synaptic strength. Many studies have demonstrated that these synapses have the ability to strengthen or weaken on account of synaptic activity. In other words, an increase in synaptic activity will further strengthen that connection, making it more sensitive to a particular stimulus. Conversely, a decrease in synaptic activity will weaken the connection such that it loses its sensitivity to a given stimulus. The neuronal events that result in the strengthening or weakening of a synapse are explained through two mechanisms – Long-Term Potentiation (LTP) and Long-Term Depression (LTD). In fact, scientists believe that the coupling of these two mechanisms essentially contributes to memory and learning of an individual.

Cognitive function depends on proper wiring and functional connections within neuronal circuits. Despite advances in understanding human aging and aging-associated cognitive decline, molecular and cellular mechanisms underlying aging associated impairments in learning and memory are still poorly understood. In particular, very little is known about whether physiological and molecular changes in identified neurons that are important for learning lead to aging associated decline in long-term memory storage. We approach this problem by delineating the aging associated changes in two well characterized neurons, presynaptic LE sensory neurons (LESNs) and postsynaptic L7 motor neuron (L7MN) of Aplysia whose normal functioning is critical for the learning of gill withdrawal reflex (GWR). Along with us, others have used Aplysia as a model to understand aging associated changes in neuronal physiology, response to neurotransmitters, gene expression and behavioral learning. In a study that examined electrophysiological and gene expression changes in identified neuron R15 of Aplysia, we recently described specific changes in burst firing and action potentials, expression of several genes in R15 during aging and specific changes in the expression of key regulators of transcription and translation in four identified neurons (L7, L11, R2, R15) of Aplysia. The long-term goal of this project is to identify synaptic

The brain ages just as our body ages; its ability to function and physical appearance change over time. Physical changes to the brain often include shrinking and death of neurons, decrease in neurotransmitter synthesis and signaling, and decrease in cortical thickness. The hippocampus, nucleus accumbens, and thalamus experience the most significant variances in the aging brain. These three regions can account for up 25-100% of the cognitive variance seen when comparing aged and younger individuals. Additionally, the brain can have losses of up to 50% of myelinated

Although there are many factors that influence an individual’s ability to learn, the most biological support for the process of learning involves the strengthening and weakening of synaptic connections in the brain. These processes, termed long-term potentiation (LTP)

The neurological deficits of aging may be viewed from a developmental perspective. That is, the decline in functional efficiency and deterioration of highly specialized non-dividing neuronal cells is the end point of a maturation process that occurs throughout adult life. Involution to senescence is a normal, inevitable, and inexorable physiological march; the end phase of which is expressed in generally predictable and specifically unpredictable ways. The earliest of these developmental changes occurs long before senescence and the effects of these physiological events quietly accumulate toward expression late in life.

Craft, J Gordon, C 2011, ‘Alterations in neurological function across the life span’, in J Craft, C Gordon, A Tiziani (eds), Understanding pathophysiology, Elsevier Mosby, Chatswood, NSW, pp. 188-226.

As people age the reaction time significantly deteriorates causing slower stimulus responses. Seen in figure 1, the values displayed a direct relationship, which showed reaction time worsened with age. This may be due to the “white” matter also known as the myelin sheath is slowly dispersing, this then may lead to slower brain power. The myelin sheath which creates faster brain access for neurons, gradually exacerbates with age because between the age brackets of 0-30 the brain is at full arousal but after the age of 30 the brain starts to slowly degrade, causing lose of power and speed to respond quickly. This clearly showed that reaction is heavy associated with age. Another trend seen in the graph is that between the age of 30 and under

The authors of this study wanted to investigate how caloric restrictions and exercise affected the synaptic alterations. They knew that caloric restriction and exercise help in the aid of extending a person's lifespan and at the same time mitigating age-related changes. In their study, the authors hypothesized that by changing or altering the synapses itself through form of diet or exercise, they can prohibit or control age-related changes entirely. In order to do so, they examined the structure of synapses, particularly skeletal neuromuscular junctions (NMJs). To test their hypothesis, they ran experiments and studies on various ages of mice, to determine the various concentrations of Acetylcholine receptors (AChR’s) that were labeled with

Why does the human brain age? Brain aging is a part of human life and a big part of society as the awareness for brain aging increases. Over time memory tends to become less efficient as we age and the neurons in the brain decreases (Bendheim, P.E. (2009). By 2050 in the US, 20 percent of the population will be 65 years or older. And as the elderly population increases, so will the incidence of age-related neurological disorders (Perlmutter, David. (2004). Therefor it is important to understand the aging brain, and how to keep the brain functioning as one ages.

Aging causes structural and functional changes in brain. As aging population has become a burden, it is essential to study aging brain aiming to maintain cognitive integrity. Previous studies indicated that young blood improves the function of stem cells in organs including brain by heterochronic parabiosis model. However, data is lacking whether regeneration or beyond occurs by this model. The authors Villeda et al., hypothesized that aged animal exposed to young blood can counteract aging process and rejuvenate brain cognitive function. Therefore, the authors conducted research to examine within molecular, structural, functional, and cognitive aspects.

It is clear to neurobiologists that aging results in a decrease in brain size as well as a decrease in the efficiency of brain functions. It has been a widely held belief that aging causes neurons to die and for the overall number of neurons to decrease as one reaches old age. Studies