Cyytotoxicity Of Nannodisc

With Alzheimer’s disease the brain becomes smaller and has narrower gyri and wider sulci, mainly in the frontal and temporal lobes (Gould, 2011, p. 522). Alzheimer’s disease affects three processes that keep neurons healthy: communication, metabolism, and repair. There are specific nerve cells in the brain which stop working and drop their connections with other nerve cells, and then they completely die (Anderson). The death or deterioration of the nerve cells is what impairs the memory in those who suffer with Alzheimer’s disease. The plaques, which disrupt the neural conduction, contain fragments from beta-amyloid precursor protein; the role of

Alzheimer’s disease is a prominent brain disease that effects a massive amount of individuals in the United States. Alzheimer’s disease (AD) is the sixth leading cause of death in the United States, accounting for 60-80% of dementia cases, with no chance of being cured, prevented or decelerating over time (Alzheimer’s Association, 2014). AD is the most well-known form of dementia, causing complications in brain function in the areas of memory, thinking, and behavior (Alzheimer’s Association, 2014). In an effort to gain a deeper understanding of Alzheimer’s disease, researchers create new knowledge about the disease, which is then distributed to the public. The goal in this information disbursement is to find new and inventive ways to treat AD, prevent AD from progressing at such a rapid pace, and aid in the quality of life in those diagnosed with AD as well as caregivers and medical professionals providing treatment to individuals’ with AD.

Alzheimer’s disease is a complex illness that affects the brain tissue directly and undergoes gradual memory and behavioral changes which makes it difficult to diagnose. It is known to be the most common form of dementia and is irreversible. Over four million older Americans have Alzheimer’s, and that number is expected to triple in the next twenty years as more people live into their eighties and nineties. (Johnson, 1989). There is still no cure for Alzheimer’s but throughout the past few years a lot of progress has been made.

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

Dr. Longo says, “Most people are working at the edges of the problem, but we’re going right after the core of it.” His goal is keeping the brain’s nerve cells healthy and protected against any assault, including the amyloid plaques and tau tangles. He and his team have developed a drug called LM11A-13 aka C31, which is showing very promising results so far in mice, even indicating the possibility of reversing damage already done! It focuses on maintaining the health and function of the neuron, the connections between neurons and interrupting many of the unhealthy communications caused by amyloid that in turn destroy the cell. LM11A-13 has been found to be safe for humans, and trials will soon begin on Alzheimer’s patients. There are still a lot of unanswered questions, but this drug could lead to helping millions of people affected or who have the potential to be affected by this horrible disease, maybe even preventing it all together.

Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal

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

Shrinkage in parts of the brain such as the cortex and hippocampus, affects functions such as remembering, planning and even thinking. The remaining tissue contains plaque, abnormal clusters of protein fragments, between surviving nerve cells. This plague can block cell-to-cell signaling at synapses and activate immune system cells that trigger inflammation while devouring disabled cells. The dead and dying nerve cells contains tangles, which are made up of twisted strands of another protein. Tangles destroy a vital cell transport made of proteins, which block nutrients and other essential supplies from reaching cells, which then die. The progression of Alzheimer’s disease follows the spreading of plaque and tangles throughout the brain. The escalation damage areas of the brain that involve speaking and understanding speech and also the sense of where a body is in relation to surrounding objects. In severe cases of Alzheimer’s, where the cortex is intensively damaged, the brain shrinks so dramatically due to widespread cell death that individuals lose the ability to communicate, recognize loved ones, and care for

All the neurons work together like a tiny community; different groups take in information, produce energy, assemble equipment, and dispose of waste. In order for this “community” to run smoothly, the cells need to be able to handle and store information, and most importantly, correspond with other cells. Alzheimer's inhibits these cells from performing like the community; when cells incapable of carrying out their jobs, they die and cause permanent impairment to the brain. The suspected “culprits” are tangles and plaques. Plaques are accumulations of a protein particle known as beta-amyloid; these deposits concentrate in the spaces between brain cells. Tangles are contorted fibers of a different protein called tau, that collect inside the nerve cells. Plaques and tangles cut off communication among cells, thus hindering the “community” and killing

β-amyloid aggregation spread from the site of injection to include both hemispheres of the brain further displaying the potentiation induced by aggregates within the brain homogenates (Stöhr et al, 2012). Under transmission electron microscopy, purified β-amyloid aggregates from transgenic mice revealed densely bundled fibrils; which were observed to increase levels of GFAP, Aβ(1-40) and Aβ(1-42) in bigenic mice at 300 days post injection via ELISA and immunoblotting (Stöhr et al, 2012). Crude brain homogenate exhibited approximately 15-20 times less β-amyloid than the purified homogenates (Stöhr et al, 2012). BLI of bigenic mouse brains injected with purified homogenate exhibited an early time of detection with signals at 161 + 7 [Tg(APP23)] and 173 + 9 [Tg(CRND8)] days (Stöhr et al, 2012). (FIGURE). Synthetic β-amyloid aggregates, wild-type Aβ(1-40) and mutant Aβ(AβS26C)2, were used to determine if prior results from purified brain homogenate could have contained any cofactors which would affect propagation of pathology (Stöhr et al, 2012). Results from the injection of synthetic fibrils into bigenic mice revealed similar β-amyloid aggregation, however pathology was less severe than purified brain homogenates from transgenic models (Stöhr et al, 2012). BLI of synthetic fibrils revealed a decrease in

Dementia is a disease that affects a vast number of Americans, and people worldwide. As people grow and live longer in today’s world the cases of clinical dementia are increasing. There are many causes of dementia, equally leading to different forms and symptoms of this disease. Most causes of dementia are known, and labeled in order to establish proper treatment. Alzheimer’s disease is the most common form of dementia, accounting for more than half of all people with dementia. The cause, and symptoms of Alzheimer’s disease are well known within the scientific community, but a cure is yet to be discovered. This show that there is still much improvement to be done within the scientific and medical

One of the most common forms of dementia in US is Alzheimer’s disease with an estimated 5.3 million Americans with Alzheimer’s disease in 2015 and approximately 700,000 patients of age 65 and older to die of this disease. Alzheimer’s has thus become the sixth leading cause of death in the U.S. Currently, one of the top 10 causes of death in America, Alzheimer’s disease progression cannot be slowed, cured or prevented. However, various researchers have been working on methods to decrease the progression or cure the disease, primarily focusing on the potentially modifiable risk factors.

Even though scientists are unsure about the causes of Alzheimer’s disease, there have been numerous tests and studies that have gleaned some insights. Francesca Fernandez-Enright, PhD and professor of neuroscience at University of Wollongong, and Jessica Andrews, professor of neuropsychology at the University of Wollongong, characterize Alzheimer’s as the accumulation of neurofibrillary tangles and amyloid plaques in the brain” (Fernandez-Enright). Amyloid plaque is the “sticky buildup” of proteins normally found in the body that divide and create “beta amyloid which is toxic to neurons in the brain” (Myers). Amyloid plaques have “different rates of growth throughout neocortical and hippocampal regions” and are formed from the “oligomers of amyloid in the intracellular and extracellular space,” and when the oligomers accumulate they become “toxic and trigger the start of neurodegenerative processes,” which becomes Alzheimer’s disease (Fernandez-Enright). Amyloid plaque production itself is not the problem, because it is needed for healthy brain function. However, when there is too much production of the amyloids it damages the “synapses, resulting in neurodegenerative processes” (Fernandez-Enright). In addition to amyloids, a type of

Because of the lack of β-hexosaminidase A, the body cannot break down excess GM2 ganglioside and the fatty substance is able to build up profusely in the nerves and tissues of the brain.

Apart from these classic hallmarks, increasing evidence has demonstrated uncontrolled glial activation and neuroinflammation in AD brain may contribute independently to neural dysfunction and cell death (Akiyama et al., 2000; Wyss-Coray and Mucke, 2002). Robust activation of microglia has been found in and around the area of amyloid plaques in the AD brain, and reactive astrocytes have been shown to form a halo surrounding the amyloid plaques (Itagaki et al., 1989; Ho et al., 2005). Additionally, numerous proinflammatory factors have been reported to be elevated in both patients with AD and transgenic animal models of AD (Griffin et al., 1989; Akiyama et al., 2000; Ruan et al., 2009). Whether alleviation of neuroinflammation will offer therapeutic benefit for AD remains unclear. Epidemiological studies show a possible association between suppression of inflammation and reduced risk for AD (in t’ Veld et al., 2001; Vlad et al., 2008). Therefore, drugs targeting neuroinflammation might provide benefits for the prevention and treatment of this devastating disease.