fever, genetic engineering & gene theraphy

8/14/2019 Fever, Genetic Engineering & Gene Theraphy

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1. Discuss the pathogenesis of fever and acute-phase response. Show illustration

Fever definition

o Elevation of body temperature to above normal (98.40F) or 370C orally or 99.80F or 37.60C rectally)

Challenge to fever

o To establish the causative agent distinguish viral from bacterial diseaseo Identify the site of a localized infection

Illustration:

Pathogenesis of fever

Exogenous pyrogens:Microbes, microbial toxins, other microbe products

Endotoxins ( bacterial toxin)

PML, Monocytes, Macrophages

Endogenous pyrogens: IL-1;IL-6;TNF-a & IFN B and Y

Thermosensitive neurons (Anterior hypothalamus)

FEVER

Thermoregulatory responses:

Redirection of blood to and from Cutaneous vascularbeds

Increased or decreased sweating

ECF volume regulation

Behavioral changes

Why Fever Occurs

Exogenous pyrogens: e.g.infectious agents, drugs

White blood cells(macrophages, monocytes, neutrophils)

Cytokines e.g. IL-1, TNF

Hypothalamus in brain

Prostaglandins

FEVER

o Physiologic states

causing fever:

digestion

exercise

ovulation

pregnancy

warm environment

emotiono Pathologic causes

Infection

Inflammation e.g.

connective tissuedisease

Neoplasms

Vaccines

Dehydration

Common causes of fever

o Minor illness

URTI

Viral exanthems

Gastroenteritis

o Major illnesses

Bacterial meningitis

UTI

Pneumonia

Malaria

Mechanisms of a Protective

Effect of Fevero Enhanced neutrophil

migrationo Increased production of

antibacterial substances byneutrophils

o Increased production of

interferono Increased antiviral and

antitumor activity ofinterferon

o Increased T-cell proliferation

o Decreased growth of

microorganisms in iron-poorenvironment


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Pathogenesis of fever

If the body temperature is above 37,2 C and is associated with

sweating, hyperventilation, and vasodilatation in the skin, we speak offever. At the beginning, gradual increase in body temperature is observed

together with muscle shivering, vasocontriction in the skin, and

piloerection. This situation is called chills. Increased body temperature isachieved by lowered loss of heat. Vasoconstriction in the skin and

subcutaneous tissue is the cause of pale color and dryness, the affected

person has a feeling of coldness. At the same time the production of heat in the organismincreases. The muscle tonus increases, the spasms accur. Spasms may occur mainly in children.

When the vasodilatation starts in the skin, the feeling of warmth and sweating occurs.

Fever may be provoked by many stimuli. Most often, they are bacteria and their

endotoxins, viruses, yeasts, spirochets, protozoa, immune reactions, several hormones,medications, and synthetic polynucleotides. These substances are commonly called exogenicpyrogens. Cells stimulated by exogenic pyrogens form and produce cytokines called endogenic

pyrogens. Endogenic pyrogens centrally affect the thermosensitive neurons in the preoptic areaof the hypothalamus increase the production of heat and decrease in heat loss. The body

temperature increses until it reaches the set point. This information is transferred by temperature

of blood that flows around the hypothalamus. The decrease of temperature is controlled by

activation of mechanisms regulating increased outcome of heat to the surrounding area.Increased outcome continues in favourable case until the new equilibrium is achieved.

The most important endogenic pyrogens are IL-1, IL-6 and cachectin also called the

tumour necrosis factor- (TNF- ). These are glycoproteins that also have other importanteffects. They are produced especially by monocytes and macrophages but also by endothelial

cells and astrocytes. Also the interferons , and display the pyrogenic activity.

After administration an endotoxin in an experiment, the level of plasmatic TNF- increases and

fever occurs. Increased concentrations of IL-1 and TNF- are also found in sepsis. Theproduction of these cytokines is regulated by the positive feedback mechanism. Besides this,

macrophages activated by IFN- may increase the production of IL-1 and TNF- primary

induced by other stimuli. On the other hand, glucocorticoids and prostaglandins of group E may

display inhibitory effect on the production of IL-1 and TNF- . Released IL-1 and TNF- aretransported by blood. They affect the target cells in the close proximity or in distant sites. The

target cells have specific receptors for IL-1 and TNF- . In the hypothalamus, IL-1 and TNF-

trigger the synthesis of prostaglandis of group E from the arachidonic acid of cytoplasmicmembranes of target cells. Precise mechanism by which prostaglandin PGE reset the central

thermostat, is not known. Aspirin and the non-steroidal antiphlogistics display antipyretic

activity by inhibiting the cyclo-oxygenase, an enzyme responsible for the synthesis of PGE(these antipyretics don't inhibit the production of TNF- or IL-1). Glucocorticoids work

antipyretically by inhibiting the production of IL-1 and TNF- , and by inhibiting the metabolic

processes of arachidonic acid.

In the process of fever, IL-1 and TNF- play the central role. Except introducedactivity in fever, they interfere with many mechanisms in an organism. Some of their effects

are executed with the participation of metabolites of arachidonic acid. IL-1 and TNF- affect

myelopoesis, release of neutrophils and enhancement of their functions. They causevasodilatation and the increase the adhesivity of cells, increase the production of PAF and

thrombomodulin by endothelial cells, proteolysis and glycogenolysis in muscles, mobilisation of

lipids from adipocytes, proteosynthesis and glycogenolysis in the liver, induce proliferation of

fibroblasts, activate osteoclasts and the release of collagenase from chondrocytes, induce slowwave sleeping activity in the brain, the release of ACTH, beta endorfins, growth hormone and


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digestion by the macrophage before they can be recognised by the other cells of the immune

system. Bits of these materials will be displayed on the surface of the macrophage and via

contact stimulate both B and T cells into appropriate action.

Lymphocytes (including B and T cells) mainly produce immunoglobulins (antibodies)

and are also responsible for cellular immunity. Cellular immunity is involved in delayedhypersensitivity (allergies and various overreactions of the body) and homograft rejection.

Lymphocytes can also damage foreign cells (bacteria, parasites, fungi, etc.). Human lymphocytesare formed chiefly in the bone marrow. Normal T cells develop only in the presence of a normal

functioning thymus. Long lived lymphocytes are primarily T cells, that recirculate through the

spleen and the lymph nodes, thoracic duct and bone marrow, leaving and re-entering thecirculation repeatedly. There are subpopulations of T cells which serve to enhance (helper T) or

reduce (suppressor T) B-cell responses. It is not yet known precisely how the various surface

receptors on T and B cells influence cell function, but they are probably involved in antigenrecognition and cell-to-cell interactions with macrophages and other lymphocytes.

We see the various cells involved in the process under our powerful microscopes in stillpictures. We also can measure various substances at various points throughout the inflammation

process and we can identify certain specific sites on the cell surface. From this information wepiece together the story of cellular immunity. In fact, we tell a number of "separate" stories about

the immunological response. There is the story about how antibodies are first formed and then

used to illicit a rapid response when exposed to the same "intruder" again. There is the story ofhow the immune system responds to a bacterial, or similar, invasion. There is the story of how

the immune system creates tolerance for the prevention of immunologically induced self-injury.

There is the story of autoimmunity, whereby antibodies are formed against the body's own tissue,

which will consequently be attacked. There is the story of anaphylaxis, an extreme overreactionof the body defence mechanism. There is the story of the complement system, which consists of

at least 15 plasma proteins which interact sequentially, producing substances that mediate severalfunctions of inflammation. A lot of stories in which different substances and pathways aredescribed, but without any serious linking of the various stories or without any knowledge as to

why and how the body chooses to follow that particular pathway on that particular occasion.

Returning to the acute phase response, the story we are particularly interested in, we

know that there are many different cytokines (messengers) involved. One of the first cytokines tobe released by the macrophages on detecting signs of injury or infection is known as interleukin-

1 (IL-1). It diffuses into the tissue surrounding the damaged cells, where it triggers a second

wave of cytokines which cause other types of immune cells such as neutrophils and monocytesto migrate to the injured site. The IL-1 released by the macrophages also enters the blood

stream, where it is carried to the brain, but is prevented from entering the brain directly by a

layer of cells known as the blood-brain barrier. It therefore adopts a more cunning route into thecentral nervous system. First, the IL-1 molecules attach themselves to specially designed

receptors on the surface of the cells in the blood-brain barrier. When these receptors are

activated, a chain reaction is initiated that eventually leads to the manufacturing of a molecule

known as prostaglandin E2, which, unlike IL-1, is capable of passing through the blood-brainbarrier. When it enters the brain, prostaglandin E2 activates the receptors on both neurons and

microglia (immune cells in the brain), which can then initiate the other components of the acute

phase response: fever, lethargy, apathy, loss of appetite, anxiety, and increased sensitivity to painin other areas of the body. But the story does not end there. Once inside the brain, prostaglandin

E2 encourages the microglia to manufacture IL-1. The net result is that, although IL-1 cannot

cross the blood-brain barrier directly, a build-up of IL-1 in the blood stream leads to a build-upof IL-1 in the brain and the cerebrospinal fluid. To complete the cycle, the IL-1 leads to further

synthesis of prostaglandin E2 in the brain, which in turn augments the various components of

sickness behaviour.

To compensate for the decreased supply of new calories caused by the loss of appetite,the body starts to unleash old calories that have been stored up for just such times of

emergencies. These calories are stored in fat deposits around the body, but before the fat can be


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used as a source of energy it must be broken down into glucose. So another crucial component of

the acute phase response is the secretion of glucocorticoids, which trigger the process of

converting fat to glucose. The key glucocorticoid in humans is cortisol, which is released by theadrenal glands in response to a cascade of chemical signals initiated in the brain by IL-1. First,

the IL-1 stimulates the hypothalamus to secrete a chemical called corticotrophin releasing

hormone (CRH). The CRH travels to the pituitary gland, just below the brain, where it triggersthe release of another chemical called adrenocorticotrophic hormone (ACTH). Finally, the

ACTH reaches the adrenal glands, which secrete the cortisol. Because of their close

interconnections, the three anatomical structures involved in this chemical cascade are knowncollectively as the hypothalamo-pituitary-adrenal axis.

Conclusion:

Fever appears to have evolved in vertebrate hosts as an adaptive mechanism for

controlling infection. This phenomenon is produced by certain exogenous (largely microbial)

stimuli that activated bone-marrow-derived phagocytes to release a fever-inducing hormone

(endogenous pyrogen). Endogenous pyrogen, in turn, circulates to the thermoregulatory center of

the brain (preoptic area of the anterior hypothalamus) where it causes an elevation in the "set-point" for normal body temperature. Warm blooded animals produced fever by increasing heat

production (through shivering) or reducing heat loss (by peripheral vasoconstriction), whereas

cold blooded animals do so only by behavioral mechanisms (seeking a warmer environment).

Fever is a part of the acute phase response to infection and inflammation. We now

understand that fever is a complex physiological response that is aimed at facilitating survival of

the host. The fever is induced by endogenous inflammatory mediators, such as prostaglandins

and pyrogenic cytokines, that are released by immune cells activated by exogenous pyrogens.

Although the pathways (humoral and/or neuronal) responsible for transfer of the pyretic signals

from the blood to the brain are still under discussion, it is generally accepted that they act on the

level of the anterior hypothalamus to raise the thermoregulatory set-point. Results of studies of

the adaptive value of fever demonstrate an association between a rise in body temperature and a

decrease in mortality and morbidity during infection. These data along with data from

evolutionary studies provide a strong support for the concept that fever is a beneficial during

infection in endotherms and ectotherms, vertebrates as well as in invertebrates. There are also

evidence showing that fever may be used as a therapeutic tool, especially in cancer therapy.

Fever has evolved as a host defense mechanism which was preserved within the animal kingdom

through hundreds of millions of years of evolution.


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The Immune System

In relation to infection & inflammation to Fever

There are physical, chemical, and cellular defenses against invasion by viruses, bacteria, and

other agents of disease.

During the early stages of an infection, there is an inflammatory response

Non-specific attack

Phagocytes active ("eat" pathogen)

During later stages, leucocytes produce immune responses

Antigen - a foreign substance which triggers an immune response Some WBC's produce antibodies in huge amounts

o Antibodies - substances which bind to specific antigens and tag them for

destruction

o Other WBC's (executioner cells) directly destroy body cells

Surface coverage - the first line of defense

The body is protected from pathogens by the skin and mucous membranes

o Skin - dead cellular layer - dry, low pH

o Mucous membranes contain lysozymes (enzymes which break down bacteria)o Other cells contain cilia which filter pathogens and particulates

Breaks in the protective barrier

o Digestive openings

o Reproductive openings

o Respiratory openings

o Sensory Organs

Non-specific responses - the second line of defense

Non-specific responses are generalized responses to pathogen infection - they do nottarget a specific cell type

The non-specific response consist of some WBC's and plasma proteins

Phagocytes - cells which "eat" foreign material to destroy them

o Phagocytes are formed from stem cells in bone marrow (stem cells are

undifferentiated WBC's)

Neutrophil - phagocytize bacteria

Eosinophils - secrete enzymes to kill parasitic worms among other

pathogins Macrophage - "big eaters" phagocytize just about anything
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Macrophage destroying bacterial cells

Non-phagocytic leucocytes -

o Basophil - contain granules of toxic chemicals that can digest foreign

microorganisms. These are cells involved in an allergic response

o Mast Cells - similar to basophils, mast cells contain a variety of inflammatorychemicals including histamine and seratonin. Cause blood vessels near wound toconstrict.

Complement proteins - plasma proteins which have a role in nonspecific and specific

defenses

o Form a cascade effect - if only a few are activated, they will trigger others to

become active in great numbers

Some punch holes in bacterial walls (forms holes where cellularcomponents leak out)

Some promote inflammation

Concentration gradients attract phagocytes to irritated or damagedtissue
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Encourage phagocytosis in phagocytes (promotes "eating")

Some bind to the surface of invading organisms

Chemokines - create a chemical gradient to attract neutrophils and other leucocytes to

the wound site

Inflammation

o

Causes localized redness, swelling, heat, and paino Changes in capillary wall structure allow interstitial fluid and WBC's to leak out

in tissue

o Promotes macrophage (phagocytic WBC's) activity

o Macrophages secrete Interleukins (communication proteins among WBC's)

Interleukin-1: increases body temperature (i.e. causes a fever)

This enhances the WBC's ability to protect the body Causes drowsiness - reduces the body's energy usage and stress

The Immune System (Specific Responses) - the third line of defense

Called into action when nonspecific methods are not enough and infection becomes

widespread

Types of cells involved in the immune system:

Macrophages - engulf foreign objects

o Inform T lymphocytes at a specific antigen is present

Helper T cells - produce and secrete chemicals which promote large numbers of effector

and memory cells

Cytotoxic T cells - T lymphocytes that eliminate infected body cells and tumor cells

B cells - produce antibodies (secrete them in the blood or position them on their cellsurfaces)

Each type of virus, bacteria, or other foreign body has molecular markers which make it unique

Host lymphocytes (i.e. those in your body) can recognizeselfproteins (i.e. those which

are not foreign)


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When a nonself(foreign) body is detected, mitotic activity in B and T lymphocytes is

stimulated

o While mitosis is occurring, the daughter populations become subdivided

Effector cells - when fully differentiated, they will seek and destroy

foreign

Memory cells - become dormant, but can be triggered to rapid mitosis ifpathogen encountered again

Thus, immunological specificity and memory involve three events:

(1) Recognition of a specific invader

(2) Repeated cell divisions that form huge lymphocyte populations

(3) Differentiation into subpopulations of effector and memory cells

Antigen - a nonself marker that triggers the formation of lymphocyte armies Antibodies - molecules which bind to antigens and are recognized by lymphocytes

Antigen-presenting cell - a macrophage which digests a foreign cell, but leaves the antigens

intact. It then binds these antigens to MHC molecules on its cell membrane. The antigen-MHC

complexesare noticed by certain lymphocytes (recognition) which promotes cell division(repeated cell divisions)

Molecular cues that stimulate lypmphocytes to create an immune response

T cells (Helper T cells and Cytotoxic T cells)
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T cells arise from stem cells in the bone marrow - they then travel to the thymus where

the differentiate and mature. At maturity, they acquire receptors for self markers (MHC

molecules) and for antigen-specific receptors. They are then released into the blood as"virgin" T cells.

T cells ignore other cells with MHC molecules and they ignore free-floating antigens.

However, they will bind with a antigen-presenting macrophage (a macrophage possessinga MHC-antigen complex). This binding promotes rapid cell division and differentiationinto effector and memory cells (all with receptors for the antigen)

Effector helper T cells secrete interlukins (stimulate both T and B cells to divide and

differentiate)

Effector cytotoxic T cells recognize infected cells with the MHC-antigen complex. They

then destroy the cell with perforans (enzymes which perforate the cell membrane,

allowing cytoplasm to leak out) and other toxins which attack organelles and DNA

Cell-mediated immune response

B cells and Antibodies

B cells also arise from stem cells in the bone marrow. As they develop and mature, they

start synthesizing a single type of antibody

Antibodies are proteins which recognize antigens

The virgin B cell produces antibodies which move to the cell surface and stick out

The B cell floats in the blood - when it encounters the specific antigen it becomes primed

for replication

The B cell must receive an interleukin signal from a helper T cell which has already

become activated by a macrophage with a MHC-antigen complex. This promotes rapid

cell division.

The B cell population then differentiates into effector and memory B cells

The effector B cells then produce a staggering amount of free-floating antibodies

o

When these free-floating antibodies encounter an antigen, they tag it fordestructionby phagocytes and complementary proteins

o These types of responses are only good for extracellular toxins and pathogens -

they cannot detect pathogens or toxins located inside of a cell
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Antibody-mediated immune response

Where do all of these interactions take place? - In the lymph nodes.


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2. Explain the role of genetic engineering and gene therapy in the treatment of neurological

disorder.

Genetic engineeringis the process of inserting new genetic information into natural cells

for the purpose to modify a specific organism by altering or enhancing genes. Since the 1970s,

scientists have genetically engineered animals to repair genetic defects and enhance their

resistance to disease. Today, scientists genetically engineer animals to enhance their production

of useful substances that provide nutrition or treatment medication for humans. For example, a

sheep named Tracy was genetically enhanced to produce large quantities of human protein in her

milk. Similar to Tracy, cows are also being enhanced to produce extra proteins in their milk to

improve the nutritional value. A Hen named Brittany was also one of the first animals to be

genetically engineered. She was modified to produce eggs with high levels of protein, which are

useful to create anti-cancer drugs. Also, plants are genetically engineered for similar reasons. In

particular, they are enhanced to increase crop yields, crop quality (redness of a tomato, prolong

freshness), tolerate environmental extremes (cold, dry weather) and have greater resistance to

disease and pests.

As science around genetic engineering develops, humans may one-day be able to design

their children. Today, scientists hold the science to enhance the intelligence of animals, which

brings anticipation for future procedures on humans. Joe Tsien, a Princeton University

Neurobiologist, genetically engineered a single gene called NR2B into mice to control a brain

chemical called NMDA (N-methyl-D-aspartic acid) that plays a role in learning and memory.

Tsiens results showed that after the gene was inserted into the mice, they produced more

NMDA. To prove that these mice attained enhanced intelligence, Tsien and his colleagues tested

the abilities of these mice compared to unmodified mice. These mice were put to tasks such as

recognizing objects in their environment and solving problems such as how to get out of water

and or off a high shelf. As a result, the genetically modified mice outperformed the unmodified

mice Tsien concludes that these findings suggest that enhancing the intelligence of humans may

be possible. He explains that the gene in humans that corresponds with memory and learning has

been found and how it performs in the brain is currently being studied.

Gene therapy is a medical procedure that may hold the cure for many of the diseases and

disorders of humankind. Gene therapy, a rapidly growing field of medicine, is the insertion of

genes into a persons cells and tissues to treat an inherited disease. It is much like a transplant.

However, although transplanting a human heart or liver is complex, transferring genes involves

thousands of small molecules that cannot be seen with even the most powerful of microscopes.

Gene therapy aims to supplant a defective mutant gene with a gene that works. The technology is

still in its infancy but has been used with some success although many questions still surround

the procedure. To understand gene therapy, it is first necessary to understand heredity.


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Neurological conditions were once thought to be off-limits to gene therapy approaches

because of the bloodbrain barrier. However, genetic research activity in this area is progressing.

Scientists are investigating the possibility of gene therapy to treat Alzheimers disease, epilepsy,

Parkinsons disease, and other neurological diseases.

ALZHEIMERS DISEASE (AD)

Gene Therapy and AD

In 2006 researchers at the Salk Institute and the University of California, San Diego, have

used gene therapy to reduce memory loss in mouse models of AD by reducing the amount of an

important enzyme -secretase, or BACE1. According to Oded Singer, one of the authors of the

study, mice with AD overcame deficits after progressing to a severe level of the disease. This

finding is important because humans are usually not diagnosed until the disease has progressed

into recognizable stages. However, amyloid plaques can precede the onset of dementia by many

years. Enzymes cut the APP and release toxic fragments that stick together to form clumps. One

of the enzymes that damage APP is-secretase or BACE1.

Gene theraphy for alzheimer

They located the forebrain, where memory cells are held, and injected it

with 40 billion viruses through holes drilled on either side of the upper skull. The vector viruses went into the memory cells and released DNA into the

nucleus.

The DNA produced NGF.

NGF (nerve growth factor) was then released to the rest of the brain to maintain cells important

to memory.

EPILEPSY

On 8 November 2006, researchers at the Childrens Hospital of Philadelphia announced

that they had inhibited the onset of epilepsy after a brain insult in animals. A brain insult is an

initial episode of epilepsy or an injury such as a severe head trauma; the patient often develops

epilepsy after such insults.

Using gene therapy to modify signaling pathways in the brain, neurology researchers,

Amy R. Brooks-Kayal and her colleagues significantly reduced the development of seizures in

rats. Seizures are caused by the rapid firing of brain cells and are thought to be caused by an

imbalance between the neurotransmitters and the glutamate system, which stimulates neurons tofire, and the neurotransmitter gamma-aminobutyric acid (GABA), which inhibits that brain

activity. Working in a portion of the brain called the dentate gyrus, the scientists focused on type

A receptors for GABA. GABA(A) receptors are made up of five subunits of proteins that play an

important part in brain development and controlling brain activity. Rats with epilepsy had lower


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associated with L-Dopa. ProSavin is administered locally to the striatum area of the brain and

delivers genes for three enzymes that are required for the synthesis of dopamine. Oxford

BioMedica plans to start European phase I and phase II trials in 2007 in patients with late-stage

PD, and proposes a clinical plan to follow in a phase III trial, which could begin in 2009. A

different perspective on PD was published in the November 2006 issue of the British journal

Lancet Neurology. H. C. Fung and colleagues announced that there does not appear to be a gene

that strongly influences the risk of PD in most patients, although genes of small influence may

still be discovered.

Conclusion:

Advances in molecular biology have triggered an

unprecedented expansion of knowledge about human

genetics. The rise of new genetic technologies, and their

implied power, has engendered concerns among religious,

scientific, and civic leaders that these new technologies may

be growing more rapidly than our ability to prudently control

and productively use them. The ability to insert human genes

into human patients to treat specific genetic diseaseshuman

gene therapy and genetic engineering engineering ofhumans has been one of the concerns noted by those

observing the evolution of genetic technologies.

Human gene therapy will first be considered in a clinical situation where it might be

possible to treat with a human gene an individual patient suffering from a genetic disease. Gene

therapy would be attempted only when there is no other therapeutic alternative, or when the

alternatives are judged to be of greater risk or less potential benefit. Application of gene therapy

for a human genetic disease should require evidence that it is safe, might prove beneficial, is

technically possible, and is ethically acceptable. Judgments should be made in a procedurally

sound and objective regulatory framework.

Genetic engineering and gene therapy plays a role in the treatment of neurological

disorders. Making some adjustment or articulation in the genes of a human being can make a big

difference in health and well being of a person. Gene therapy could even enhance memory of an

Alzheimers patient, prevent & control seizure (Epilepsy), relieve symptoms of Parkinson

disease and even prevent further damage of the brain. Studies also show that genetic engineering

could enhance intelligence of a person based on the experiment done to a rat. Our technology

has gone so far. We have benefited a lot in our technology but it doesnt stop here because it is

continually being developed to help uplift our lives. Hope we could use the new discoveries in a

good way so that there will always be a positive outcome. We should not abuse it instead we

must use it for the improvement of our life and better health.

fever, genetic engineering & gene theraphy

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