Amyloid Precursor Protein Essay

Using these three articles (or more), you should tell the story of the discovery and developmental function (including the relevant signaling pathway) -

The purpose of this essay is to explain the mechanisms of neural communication, and the influence that different drugs have on this communication. The nervous system is made up of several cells that are called neurons, which are situated inside the Central Nervous System (Martin, Carlson & Buskit, 2013). Neurons comprise of three mechanisms, a cell body which is referred to as the soma, dendrites and an axon (Pinel, 2011).

It is a disease that we haven’t cured yet but instead have only come up and still coming up with treatment strategies to alleviate its symptoms. AD was first described in 1906 by a German psychiatrist by the name of Alois Alzheimer whilst he was performing a histophathologic study of his patient’s brain, a patient who had been suffering from dementia. His patient’s brain’s autopsy brought to light the presence of two types of lesions, which are senile plaques and neurofibrillary tangles. He saw a visible difference in the brain tissue for it was severely damaged by these lesions. Since then, our knowledge of AD’s cellular and molecular alterations has increased and we have come up with various hypotheses for AD that may soon help in developing effective preventative and therapeutic strategies. One of the most prevailing hypotheses that have already leaded to a number of therapeutic approaches is the amyloid cascade hypothesis. Hence, the following essay will explore the pathology of the amyloid cascade hypothesis and the evidence for and against it. It will also touch upon current progress in clinical trials that test the

What is Alzheimer’s? It is characterized by plaques and tangles in the brain. According to Alzheimer's association Plaques are “microscopic clumps of a protein fragment called beta-amyloid” (Alzheimer's Disease & Dementia.) The tangles are another protein called tau that is twisted. When the proteins are twisted they are not able to receive proper nutrients. The cells start to decline and not work as well, and they eventually die. The tissue that the cells make up deteriorate and the person begins to lose memory and some brain activity. This is a fatal disease and no cure has been found yet.

Alzheimer’s is a neurological brain disease that makes a person suffer in their late term of life. Alzheimer’s has two variants, early onset and late onset and they are both triggered by different genes. 95% of Alzheimer’s is in the form of late onset NIH. (2013, May 1). There are between 2.4 and 4.5 million Americans affected by Alzheimer’s today. Throughout a person’s life, the risk increases with age. There are differences between the late and early variants of Alzheimer's.

     In Alzheimer’s disease, there are three rare genetic syndromes that cause people to develop the disease before the age of sixty. These syndromes are caused by mutations in single genes call APP, PS1, and PS2. These mutated genes are usually inherited by one’s parents and virtually guarantee the development of Alzheimer’s disease. Genetic testing is currently available for these mutations and could prove to be extremely helpful in taking early action against the disease.

In 1901 Dr. Alois Alzheimer, a german psychiatrist, first described the symptoms of Alzheimer’s disease. A specific type of dementia that irregularities in the brain's structure destroys important mental functions and memory in elderly people. This type of disease has many symptoms that mainly target cognitive functioning. There is currently no cure for alzheimer's but medication can be used to slow down its progression. This disease is considered datal and it a major focus of research efforts.

Alzheimer’s disease (AD) is a slow-progressing neurodegenerative disease that has no cure and most often affects people over the age of sixty-five. Neurodegeneration is characterized by the loss of function in the central nervous system due to degeneration of neurons found mostly in the brain. The most recent data from the Center for Disease Control and Prevention shows that AD is the sixth-leading cause of death in the United States. The cause of Alzheimer’s is still not completely understood, but the current theory is that it appears to be genetic in which many genes are involved. AD is also the most common form of dementia and accounts for 60-80% of cases (Alzheimer’s Association 2016). Dementia is not a disease itself, but instead is characterized by a group of symptoms that is caused by brain disease or injury in which memory, personality, and reasoning skills are affected.

Alzheimer’s is a common disease. More than three million cases of Alzheimer’s come up each year. People of age sixty years and older are largely affected, with rare genetic changes connected to the early start of Alzheimer's

Alzheimer's disease is characterized by the formation of amyloid plaques and neurofibrillary tangles in the cortex, entorhinal cortex and hippocampus of the brain causing neuronal cell death, dysfunction of neurotransmitters (acetylcholine, serotonin, and norepinephrine) and atrophy in affected areas. B Amyloid plaques are described as insoluble clumps of peptides resulting from the cleavage of amyloid precursor protein. Neurofibrillary tangles result from destruction of neuronal microtubules which are key components of neuronal cell structure as they deliver nutrients and assist with synaptic

DRG isolation, plating, and axon elongation: Adult DRG from C1 to L1 will be dissected from SD rats ≥ 8 weeks of age using standard techniques.14,32,33 Dissected DRGs are treated in 0.25% collagenase-P (Boehringer Mannheim) in Neurobasal media (Invitrogen) for 1.5 hours followed by a treatment in 0.25% trypsin in cell dissociation buffer for an additional 1.5 hours. After trypsin inhibition, the pellet will be resuspended in complete medium and mechanically separated using a fire polished pasture pipet until the DRGs are completely dissociated. The DRG cells will be plated along the elongation interface and maintained in complete growth medium consisting of Neurobasal Media supplemented with B27 (Invitrogen), 1% FBS (Hyclone) and 1mM L-Glutamine (Invitrogen), 2.5g/L glucose, and 10μg/mL 2.5S nerve growth factor (Becton Dickinson). After cells attach, DRG cultures will be immediately treated with mitotic inhibitor cocktails consisting of 5 μM cytosine arabinoside, 20 μM 5-fluoro-2’-deoxyuridine and 20 μM uridine. Five days after plating, the axon fascicles spanning the two overlapping membranes will be elongated. Stretch-induced axon elongation is controlled by

Neurological disorders such as Alzheimer’s disease, autism spectrum disorders (ASD), and schizophrenia impact behavior and cognitive processes. While the symptoms for these diseases vary, they share disruptions in synapse development and spine formation. In the mammalian nervous system, dendritic spines are small, dynamic protrusions on neurons that develop in response to increased presynaptic activity. Although spine dynamics throughout development have been well studied, very little is known about the genes involved in spine formation. A recent study in our laboratory discovered spiny projections on a group of inhibitory neurons called DD neurons in C. elegans. Using C. elegans as a model system, the goal of this project is to identify genes responsible for dendritic spine formation. Specifically, I will 1) conduct a forward genetic screen and examine candidate axon guidance molecules to identify genes involved in dendritic spine formation, and 2) examine the effect hyper- and hypo-presynaptic activity has on the development of spines using locomotory changes, such as thrashing and microfluidic assays, and cell-specific changes using channel rhodopsin and temperature sensitive alleles. Given the strong homology between C. elegans and mammalian genes, this research will help identify conserved mechanisms underlying spine formation and maintenance. Ultimately, understanding spine development will help shape the treatment and prevention of

Irene Gutierrez thesis aims to understand the role of Shh in two very important aspects of brain development:

Alzheimer's Disease Alzheimer’s Disease (AD) is a progressive degenerative disease of unknown aetiology, as first described by Alois Alzheimer (1907). According to Shoenberg et. al (1987), it is the commonest cause of dementia in the elderly with an incidence ranging from 2.5 to 5 per thousand.

Autosomal dominant mutations in APP, PSEN1, or PSEN2 that alter APP processing and the production or self aggregation of Aβ, promote aggregation and accumulation of Aβ in brain causing early-onset AD (Bertram et al., 2010).