Gene And Microglia Mediate Early Synapse Loss Essay

New evidence states a viral infection brings Alzheimer’s to light. A recent editorial from the Journal of Alzheimer’s Disease shifts focus from immune system suppression to a viral infection. Dr. Douglas Kell, a professor at the University of Manchester’s School of Chemistry, claims, “We are saying there is an incontrovertible evidence that Alzheimer’s disease has a dormant microbial (viral) component. We can’t keep ignoring all of the evidence” (Knapton). Viruses are commonly found in the brains of elderly people. In most cases, they have all of their bodily functions. Around two-thirds of people will contract the viral infection herpes at some point in their lifetime. Herpes has been known to damage the central nervous system in humans.

Alzheimer’s disease is an irreversible, neurodegenerative disease that affects the brain causing progressive memory loss and destroys thinking skills. Alzheimer’s is the most common type of dementia, which is a general term used to describe disorders that affects brain functions. Alzheimer’s disease is caused by formations of plaques and tangles in the brain. A dangerous protein called beta-amyloid tends to build up over time in the brain. As this protein molecule accumulates, they start to form plaques, which can damage and destroy brain cells. While plaques affect the spaces between the brain cells, an abnormal protein known as “tau” starts affecting inside the brain cell itself. “Tau tangles can interfere with the transportation of nutrients in and out of the cells, causing brain cells to degenerate and die” (Kosik & Bowman, 2015, p. 5). Some common symptoms for Alzheimer’s include memory loss, constantly misplacing things, unable to remember the names of family members, unable to communicate properly, and losing the ability to complete simple daily tasks. Alzheimer’s disease is a fatal disease, but patients don’t die from the disease itself. Advanced Alzheimer’s increases vulnerability and increases the chance of developing infections that soon lead to death.

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Cognitive impairment associated with Alzheimer’s disease occurs when synapses, which transmit information from one neuron to another, become interrupted and communication ceases (7). The result is death of the nerve cell within the brain, also referred to as synaptic failure (6). Synaptic failure takes place when amyloid plaque and neurofibrillary tangles develop (7). Amyloid plaque develops from amyloid beta proteins, which are released by enzymes from the amyloid precursor protein that is located on the surface of the neuron (7). The amyloid beta proteins are normally cleared within the body once they are released however, in

Alzheimer 's disease is a progressive, degenerative disorder that attacks the brain 's nerve cells, or neurons, resulting in loss of memory, thinking and language skills, and behavioral changes. These neurons, which produce the brain chemical, or neurotransmitter, acetylcholine, break connections with other nerve cells and ultimately die. For example, short-term memory fails when Alzheimer 's disease first destroys nerve cells in the hippocampus, and language skills and judgment decline when neurons die in the cerebral cortex. Two types of abnormal lesions clog the brains of individuals with Alzheimer 's disease: Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tangles—insoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. Although these structures are hallmarks of the disease, scientists are unclear whether they cause it or a byproduct of it. Origin of the term

Alzheimer’s is a chronic and organic mental disorder discovered by a German neurologist named Alois Alzheimer. In 1906, Dr. Alzheimer began to notice changes in the brain tissue of a lady who had died of unusual mental illness. After her death, he examined her brain and found a lot of abnormal clumps and tangled fibers. The human brain has 100 billion nerve cells, and each one of them connects with a lot of others to form communication networks. Gatherings of nerve cells have certain jobs. To be able to do this, brain cells operate like small factories. Cells function and store information and communicate with the other cells. Keeping all the things going right requires coordination as well as huge amounts of oxygen and fuel. Scientists believe

Contrary to what many people believe, getting Alzheimer's is NOT a normal or natural part of aging. Yet, each year, there are more than 3 million people in the US diagnosed with Alzheimer's. Although, there is no real “cause” for this disease, factors that may contribute to it include age and family history, environmental components, particular genes (APOE-e4 or ADAD are the strongest risk genes), immune system complications, and protein deposits located in the brain. Therefore, since there is

In general, each neuron releases a single type of neurotransmitter. Neurons that release the neurotransmitter acetylcholine are called cholinergic neurons and degeneration of cholinergic neurons in the brain are associated with Alzheimer’s (Sherwood). Drugs classified as short-term cholinesterase inhibitors are used to treat Alzheimer’s because the drugs prolong the effect of acetylcholine. There are special cells called microglia that are associated with Alzheimer’s disease as well. Microglia are immune defense cells in the CNS (central nervous system) or brain and spinal cord. The remove foreign and degenerate material in the CNS. Overactive microglia appear to be involved in a variety of inflammation-related disorders like Alzheimer’s (Sherwood). Inflammation is triggered by the body’s immune system and is a factor that plays in the progression of the disease (Alzheimer’s Disease & Dementia).

At adult normal physiological condition, microglial display surveillance or so-called ‘resting’ phenotypes gauged by small cell body with extensively ramifying processes that actively surveying the CNS microenvironment. In this steady state, the turnover processes is primarily confined and well-maintained through local self-renewal of the long-lived resident microglial. Anomalies in the CNS such as infections, tissues damage, and accumulation of abnormal protein or biochemical can trigger microglial activation and in turn cause inflammation in CNS. Different from steady state, inflammatory condition may have disrupted the integrity of blood brain barrier and allowed recruitment of circulating myeloid cells and promotes their differentiation into microglial with more potent inflammatory properties and resulting heterogeneity of microglial . Activated microglial rapidly proliferate undergo phenotypic transition where they will exit from the ‘resting’ or ‘surveying’ form and mounted inflammatory effectors functions. Evidences showed that activated microglial capable of upregulated its phagocytose properties and secrete of inflammatory mediators chemokines, cytokines, nitrite, reactive oxygen species, and free radicals to execute repair

Researchers from the University of Wollongong in Australia have found a link between the ATP-binding transporter A7 (ABCA7) and the regulation in the risk of Alzheimer’s disease. ABCA7 helps to clear out Aβ (amyloid beta) from the brain. Aβs can group together and block cell-to-cell signaling at synapses. The evidence in human and mouse trials have shown that ABAC7 has a role in the regulation of Alzheimer’s treatment and risk. ABCA7 has been found to be in high amounts amongst microglia in the brain and directly regulates phagocytosis. Further testing was done to determine what the exact link is between this transporter and Alzheimer’s disease.

Alzheimer’s disease is not something we can control. The disease is a progressive, permanent, and overwhelming brain illness that causes cognitive decline, including memory, language and thinking problems. After many decades of trying to find a cure, there still isn’t one, although researchers continue to make progress. “It is unknown what causes Alzheimer’s disease but older age and family history appear to play a role” (Shu, 2011). Not only do age and family history play a factor in Alzheimer’s disease, changes to the immune system can also play a part. This could play a large role in why we do not have a cure, because we do not know, with certainty, what causes it.

Alzheimer’s disease looks to be caused by an accumulation of neurotoxic proteins in the cerebrum, this is the part of the

The brains of people with Alzheimer’s disease have an abundance of two abnormal structures – amyloid plaques and neurofibrillary tangles. These are made of misfolded proteins which can stick together with other misfolded proteins to form insoluble aggregates. If these aggregates build up, they can disrupt cellular communication and metabolism. The third main feature of Alzheimer’s is the loss of connections between cells leading to the ill-functioning and death of cells (Institute and Aging, 2011).

Alzheimer’s disease was first defined in 1906 by Alois Alzheimer, a German psychiatrist and pathologist. Alzheimer spent many years observing a middle-aged woman whose memory and cognitive abilities were quickly deteriorating. Shortly after her death, Alzheimer studied portions of her brain under a microscope, where he soon unearthed a plethora plaque deposits. He also discovered that the fine inner structure of the nerves in different brain regions were aggravated, forming tangles made up of a protein called tau (1). These discoveries lead to the socially accepted disease that we know today as the Alzheimer’s Epidemic.

Microglia stimulation initiates an inflammation cascade which involves NF-κB. The studies show that inflammation and the transcription factor nuclear factor kappa B (NF-κB) is a protein complex that controls transcription of DNA, cytokine production and cell survival, it is also implicated in synaptic plasticity, memory and learning.