Drosophila Summary

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

Introduction: The intention of this lab was to gain a better understanding of Mendelian genetics and inheritance patterns of the drosophila fruit fly. This was tasked through inspecting phenotypes present in the dihybrid crosses performed on the flies. An experimental virtual fly lab assignment was also used to analyze the inheritance patterns. Specifically, the purpose of our drosophila crosses is to establish which phenotypes are dominant/recessive, if the traits are inherited through autosome or sex chromosomes and whether independent assortment or linkage is responsible for the expressed traits.

Luckily, there are biotechnology companies trying to solve the growing problems that Alzheimer’s disease is presenting to the public. Despite repeated failures in clinical trials, leading pharmaceutical companies continue to invest time and capital in finding Alzheimer’s disease treatments. 99 percent of therapies in the past decade have come up short. Scientists are bitterly divided on the issue of targeting amyloid to effect the progression of

Heterozygotes, which have the wild type phenotype, have normal sight which gives them the advantage of finding a mate and have a better success with attracting a mate with their courtship song (Kyriacou et al, 1978). The male heterozygous Drosophila had a better advantage at mating than the homozygotes, which were the ebony, and therefore we predict there will be more wild type by the end of the experiment.

There are more than 5 million people in the U.S. with Alzheimer’s and it causes 500,000 deaths a year in the U.S. alone. This disease is growing quickly, by the year 2050 it is expected that there will be 16 million people diagnosed with it in the U.S. and 100 million worldwide. The goal is to overcome this disease by the year 2025, which is possible, but very challenging. A neurologist at Harvard Medical School, by the name of Rudolph Tanzi said, “We will be able to identify those most at risk based on their genetics, do imaging tests to determine the onset and then institute therapies that nip it in the bud”(Marsa). This is great news because it will help the doctors get a jumpstart on those who are at risk of getting the disease. Memory loss is the main issue of Alzheimer’s which is caused by tangles in the brain. Without the tangles there is no disease, the tangles are what cause it. Alzheimer’s also causes shrinkage to the brain. Moving ahead with a cure, researcher need to figure out how the protective mutant gene works, making a treatment to copy what it does

The topics include: Alzheimer’s disease and what provokes it, amyloid-beta proteins, synapses, synaptic pruning, neurons, cognitive and microglial cells. Alzheimer’s disease affects mostly individuals in their mid-60s and is “a type of dementia that causes problems with memory, thinking and behavior” (Alzheimer 's Association). The articles reflect the discovery of the Alzheimer’s disease affects the brain by the destruction of the connection of the brain cells which causes damage in neurons and accelerate cognitive decline, and occasionally call it the earliest stage. Amyloid-beta is a term that refers to the plaques made by the proteins which interferes and cause the loss of synapses also known as synaptic pruning is the loss of connections between neurons caused microglia, that according with The Campbell Biology In Focus textbook, “microglia are immune cells that protect against pathogens” (Campbell.) The authors of the research support “microglia that prune excess synapses in development are inappropriately activated and mediate synapse loss in Alzheimer’s disease.” (Taub, 2016)

As Aβ peptide, under certain circumstances, is considered an important risk factor for the onset and progression of AD. Furthermore, APP (amyloid precursor protein), which is a transmembrane protein, is expressed and metabolized at high levels in the brain and through β and γ secretase enzymes produce Aβ (Seeman et al., 2011). Consequentially, targeting these enzymes by various drugs, can lead potential therapies, which may reduce Aβ accumulation and combat AD.

Researching Alzheimer’s disease has been a continuous obstacle for all scientists. They have made miraculous advances in their

Before providing further details of Dr. Carter and her research, I would like to introduce myself. I am a Professor of Neuroscience and Neurology in the department of Neurosciences at Case Western Reserve University School of Medicine, Cleveland, OH. I obtained my B.A. in Chemistry and Biochemistry at University of Michigan in 1974, and completed Ph.D. in Neurosciences in 1979 at University of Michigan. I spent three years in Harvard School of Medicine as a Postdoc Fellow before I joined Case Western University as a faculty. I am currently a director of Alzheimer Research Laboratory and a director of the department of Neuroscience at Case Western School of medicine as well. My research interests include investigating roles of important players in Alzheimer’s disease (AD) including amyloid beta (Aβ) and apolipoprotein E (ApoE). My laboratory identifies molecular components participating in Aβ aggregation or degradation and searches for therapeutic agents to counteract the catastrophic neurodegeneration

Alzheimer’s is a slow disease, taking 8 to 20 years from diagnosis to death. The main culprit of the infamous memory- loss disease is the beta amyloid protein. This protein builds up forming plaques. Beta amyloid also attaches to neurons first blocking synapses and eventually forming tangles by killing them. Over time more and more of these plaques and tangles accumulate while killing over 100 billion nerve cells. The damage these buildups of protein cause are tragic. Physically the brain shrinks; starting with the hippocampus and slowly progressing. However the changes the person affected with the disease encounters are far worse.

Amyloid β-peptide (Aβ) is the major component of the senile plaques, and the amount of Aβ to form the plaques is correlative with the degree of neuronal damage and cognitive deficit. Although four million new cases of dementia are recognized yearly, and nearly 70% of these cases are ascribed to AD, there is still now not fully elucidated and no efficient method for its

The modification that I think would be the most popular enhancement by 2030 focuses on one section of SENS (Strategies for Engineered Negligible Senescence) research currently being explored by biomedical gerontologist Aubrey de Grey. His foundation focuses on removing, restoring, substituting, and reducing cellular and molecular damaged that impacts human tissues as we age so that humans can potentially live for centuries (“Reimagined Research”). The organization recognizes seven different areas where this research can help humans, but I want to focus on one specific biotechnology that can improve the brain. AmyloSENS is a rejuvenation biotechnology that deals with removing extracellular aggregates from various parts of the body. The most common type of malformed protein is beta-amyloid which forms plaque that

Drosophila melanogaster, which too many of us is commonly known as fruit fly, this fly although small and without much relevance in to this world contributes a major role in laboratories. Is a model organism used in the scientific research fields that relate to evolution and genetics. One of the key role that Drosophila melanogaster has is that it is commonly used monohybrid and dihybrid test crossing. As Dr. Jennings states in her article Drosophila-a versatile model in biology and medicine, “Research using Drosophila has made key advances in our understanding of regenerative biology and will no doubt contribute

The activity of an organism may be affected by different light intensities. One of the species believed to be affected by this factor is the fruit fly, Drosophila hydei (source). Based on my personal observations of the Drosophila hydei, they are approximately four millimeters in size and have a dark brown body connected to six legs and a pair of wings. A distinct and important feature of the organism in sensing light intensity are its red eyes, which are located on the sides of its head. In response, the Drosophila hydei's six thin legs are used for movement. Its pair of wings would be used in natural conditions but for our experiment we are using a mutant species which can not fly. Another feature which is not used for sensing light intensity but for hearing and smell for example, are two small antennae between its eyes.

The central role of enzymes is to function as biological catalysts. Since the fundamental tasks of a protein is to act as an enzyme, catalysts increase the rate of the activation energy within a cell. Cell contain thousands of different enzymes, and their activities determine what chemical reaction will take place within the cell. The enzyme and the activation energy function as a process within the cell, chemical reactions do not just occur spontaneously or sporadically. Enzymes control the productivity and speed of chemical reactions within our body, it’s important to understand how they catalyze and function.