Annonacin Synthesis Essay

1. Introduction

Neurobiology provides a solid foundation on which to explain the molecular pathogenesis of most chemically triggered brain diseases, including self-limiting human neurodegenerative disorders. For example, substances with neurotoxic potential may bind to membrane receptors, enter cells via membrane channels, interfere with mitochondrial function, disrupt axonal transport, or perturb synaptic integrity. The resulting neurocellular dysfunction presages functional changes that may remain sub-clinical or find clinical expression in minutes, hours, days or weeks. The associated clinical disorder peaks over time, plateaus and either persists or resolves. Thus, chemical exposure produces a self-limiting neurological disorder by activating an abnormal physiologic state that reverses or, with cell loss, persists, but does not advance. True, the neurological condition may relapse or progress in the event of continued chemical exposure or the release of an endogenously stored substance, but chemicals that act through the foregoing cellular mechanisms are considered unable to trigger a self-propelling disorder that results in the relentless, unstoppable advance of neurological disease. If chemicals are ever found to induce progressive and ultimately fatal neurodegenerative diseases, a fundamentally different neurotoxic molecular mechanism must be involved [1,2].

Ten years ago, we embarked on a voyage to discover that mechanism because of the existence of an intensively studied progressive neurodegenerative disorder that unequivocally seems to have an environmental origin and a non-infectious etiology. This fatal disease is a complex clinical mixture of amyotrophic lateral sclerosis (ALS), parkinsonism (P) and dementia (D) with a neuropathology comparable to that of Alzheimer disease (AD) [3]. The affected brain accumulates many types of abnormal intracellular deposits (synuclein, β-amyloid, TDP-43), but it is dominated by deposits of microtubule-associated protein tau (MAPT), and therefore fits into the molecular neuropathological class of tauopathies [4]. The clinical and neuropathological features of this disease are best studied among Chamorro residents of the Mariana Islands of Guam and Rota [5] and among Japanese living in the Kii Peninsula of Honshu Island, Japan [6,7]. Least studied and without neuropathologic conformation is a third isolate of western Pacific ALS-PD complex (ALS-PDC) among Auyu and Jaqai linguistic groups in the southern lowlands of West Papua, on the Indonesian side of the island of New Guinea [8,9]. These three genetically distinct groups of people have experienced an extraordinarily high prevalence of this prototypical neurodegenerative disease, the latter flourishing in a setting in which no synthetic chemicals had ever ‘set foot’ at the time of its discovery. The same disease is non-transmissible from human to monkey, in contrast to kuru, a distinct but also disappearing neurodegenerative disorder formerly found among the South Fore people in the highlands of Papua New Guinea that is believed to have an infective prion etiology [10,11].

The foregoing information suggests the operation of a naturally occurring environmental substance in the etiology of Western Pacific ALS-PDC. The only factor common to all three ALS-PDC foci is use for food and/or medicine of the seed of the hardy cycad plant (Cycas spp., Figures 1 and 2). Like all plant materials, the cycad seed is a complex mixture of chemicals, one of which (cycasin) is the principal subject of this paper. We hypothesize that the aglycone of cycasin, the potent genotoxin methylazoxymethanol (MAM), persistently perturbs cell signaling in the young adult brain because post-mitotic nerve cells are unable to repair MAM-induced DNA damage. We have solid evidence to support this conclusion for the developing rodent brain, which MAM readily disrupts, and the fingerprints of a comparable mode of action in the central nervous system of the young adult. If we are correct, MAM represents the first recognized agent with neurotoxic properties that produces a longlatency progressive neurodegenerative disease, where the interval between agent exposure and onset of neurological decline spans years or decades. We also present evidence that MAM perturbs cell-signaling pathways in the brain that are similar to those activated in mitotically-competent (cycling) epithelial cells that mutate and proliferate to form malignant tumors. This leads us to propose the possibility that cellular malignancy and progressive neurodegeneration are two sides of the same coin, the outcome depending on whether the genotoxin acts on a cycling or non-cycling cell, respectively. Since this idea deviates markedly from current understanding and has significant consequences for disease prevention and treatment, we hope our work will stimulate research on this question to prove or disprove our assertion.

We embark on this review cognizant of the incompleteness of the data we review in support of our hypothesis that unrepaired MAM-induced neuronal DNA damage perturbs cellular networks that may initiate neurodevelopmental delay in the immature brain or progressive neurodegeneration that begins in the young adult brain and appears clinically years or decades later in the form of the tauopathy ALS-PDC. Further, given the close neuropathological relationship between ALS-PDC and AD, we explore how new understanding of the former influences thinking about the possible role of environmental agents in the etiology of AD.

2. Evidence for the Role of Cycads in ALS-PDC

Since the etiology of western Pacific ALS-PDC is the subject of controversy, we should justify our position regarding the etiopathogenesis of this and other neurological diseases with which it has been compared. Several theories have been offered over the past 60+ years since high-incidence motorsystem disease was first recognized on Guam. Given its familial nature, inherited risk factors were first proposed, but with temporal decline in prevalence, some combination of genetic risk and environmental exposure was entertained. As disease rates continued to drop [12], the dominant clinical presentation changed over time from ALS to parkinsonism-dementia (PD) to Guam dementia (GD), and the age of onset continued to increase, it became increasingly clear that disease decline was most probably associated with a disappearing environmental exposure associated with the acculturation of Guam Chamorros to a western lifestyle. Screens of the Guam genome have failed to identify mutations responsible for Chamorro ALS-PDC but, in some cases, revealed polymorphisms in two independent cis-acting sites in the tau gene that might influence disease risk by regulating its expression [13]. Analysis of blood from Kii ALS-PDC subjects showed no mutations of 19 neurodegenerative disease-relevant genes [14]. Another finding in a subset of Guam ALS and PDC patients was a variant in the gene coding for the transient receptor potential cation channel, subfamily M, member 7 (TPRM7) [15], which produced functional channels with an increased sensitivity to inhibition by intracellular Mg2+ [16]. However, TPRM7 mutations have not been found in ALS-PDC cases in Kii peninsula [17]. ALS has also declined in the high-incidence disease focus of ALS-PDC in West Papua [9]. In sum, an inherited disorder is incompatible with the declining prevalence of ALS-PDC in all three geographic isolates, and no common causal genetic factor has been identified.

The longitudinal trend of ALS and PD, which has been documented epidemiologically for more than half a century on Guam, is consistent with an environmental agent that is declining hand-in-hand with post-World War II development of the island. Two hypotheses have been offered: one relates to declining use of the cycad plant for food and/or medicine [18], the other proposes that neurotoxic elements (such as aluminum and manganese) in water enter the body and are deposited in the brain. Low levels of calcium in water, it was suggested, triggered a parathyroid response that promoted gut absorption of calcium, with the result that absorption of “neurotoxic bystanders”, such as aluminum, would also take place [19]. While aluminum and other metals can be detected in the brain of Guam ALS-PDC patients, parathyroid function is unremarkable [20]. Additionally, in West Papua, ALS prevalence in a sessile, riverine population has declined without any known change in their source of drinking water [9].

The second environmental hypothesis focuses on exposures to neurotoxic components in seed of the cycad plant. The proposal originates from 1962 when the late Marjorie Whiting described the Chamorro practice of using cycad seeds for food and topical medicine [21]. Her research demonstrated that cycad plants had a long history in Australia and elsewhere of causing a neuromuscular disease in grazing animals. Cycads were found to harbor the first known plant mutagen, cycasin, and an uncommon amino acid, β-N-methylamino-L-alanine (L-BMAA), which induced an acute neurotoxic syndrome in chicks [22]. Interest in the cycad hypothesis lapsed until, decades after Whiting’s pioneering observations, we showed that primates treated orally with L-BMAA developed chronic degenerative changes in cortical and spinal motor neurons in association with a clinical picture reminiscent of the western Pacific disease [23]. However, because of the very high L-BMAA dosage used in this typical short-term toxicology experiment, and lack of disease progression after dosing ceased, the relevance of this model to ALS-PDC was subject to question. The cycad hypothesis again fell into disfavor until it was suggested the dosage of L-BMAA used in the earlier primate studies was realistic given that the Chamorro diet included flying foxes that harbored large concentrations of L-BMAA [24]. It should be noted, however, that flying foxes are not part of the diet of Japanese or New Guinean subjects at risk for ALS-PDC.

While Whiting emphasized the dietary use of cycads on Guam, the common exposure to cycad toxins in all three high-incidence disease foci is from raw cycad seed used for medicine, with the additional use on Guam of the fresh seed cover to relieve thirst, the dried seed cover as a confection, and washed but incompletely detoxified cycad ovules as a source of flour for various food products [21] (Figure 2A). The neurotoxic cycad seed has been used as a topical treatment for skin lesions large and small [25], but such use undoubtedly declined as man-made pharmaceuticals were introduced. Oral medicinal use of cycad seed was also practiced in Japanese folk medicine in the Kii focus up through the 1980s, with prescriptions written by practitioners (kitoshi) that were filled by dispensing pharmacies (Figure 2B) [26]. Repeated oral or prolonged subcutaneous application of raw cycad seed was thus common to all three ALS-PDC isolates. The Chamorros of Guam and Rota also used the cycad seed ovule as a source of food. This was not remarkable since aboriginal groups in Australia historically prepared food from carefully detoxified cycad seed ovules without precipitating recognized neurological disease. Similarly, Japanese living in the Ryukyu Islands, where ALS-PDC is unknown, employed fermentation to eliminate cycasin [27]. Guam Chamorros, by contrast, used food preparation methods that only reduced the content of cycad toxins to “edible” levels that, while not lethal, nevertheless precipitated acute illness in children likely arising from the hepatotoxic properties of cycasin. We demonstrated residual levels of L-BMAA and cycasin in cycad flour prepared by families from different Guam villages [28].

2.1. Cycad Toxins: β-N-Methylamino-L-Alanine (L-BMAA)

L-BMAA is an uncommon amino acid that is synthesized by cyanobacteria and present in seed of Cycas spp. implicated in western Pacific ALS-PDC. Whether the amino acid is an endogenous cycad product or derived from invasive cyanobacteria is questioned. It should be noted that cyanobacteria also contain genotoxins that are capable of inducing DNA damage in both human and rodent cells [29]. We showed and others confirmed that L-BMAA is an excitotoxic amino acid with acute neurotoxic properties that are attenuated by glutamate receptor antagonists. Our group and several others have shown that L-BMAA has effects on both ionotropic and metabotropic glutamate receptors [30–33].

L-BOAA is a potent stereospecific amino acid in the Grass pea that acts in micromolar concentrations as an agonist of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) class of glutamate receptors. Although small concentrations of L-BOAA are present in cycad seed, lathyrism is a self-limiting pyramidal-tract disorder quite distinct from both the clinical form and progressive nature of western Pacific ALS-PDC. In a similar vein, domoic acid, which acts predominantly as a AMPA/kainate glutamate receptor agonist [36], induces a rapid-onset self-limiting neurodegenerative disorder [37]. Based on these observations, it is unlikely that the chronic motorsystem disease induced in primates fed L-BMAA arises from a membrane-based glutamate receptor action of the cycad amino acid. Stated otherwise, if L-BMAA does have a role in the etiology of western Pacific ALS-PDC, a mechanism other than glutamate excitotoxicity must be responsible. One possibility is described in the following paragraph.

L-BMAA might exert a chronic neurotoxic effect by being incorporated into protein, the foreign amino acid residue causing protein malfunction. The basis for this hypothesis comes from experimental evidence of significant levels of protein-associated L-BMAA in washed cycad flour and the detection of L-BMAA in the brain tissue of Guam Chamorros with ALS-PDC [38,39]. In support of this hypothesis, we showed that L-BMAA, but not l-BOAA, is taken up by cortical explants and synaptosomes in a time-dependent manner [40]. Previously unpublished data confirmed tissue uptake of L-BMAA in cortical explants treated with [14C]-L-BMAA and in mouse cortical synaptosomes treated with [3H]-L-BMAA (Figure 4). Additional data (not shown) demonstrated that L-BMAA is taken up and released from cortical synaptosomes. The rapid uptake, accumulation and release of L-BMAA, but not the structural analog L-BOAA, in cortical explants and synaptosomes suggest that the sub-chronic neurotoxic effects of this excitotoxin in primates is related to unknown intracellular actions.

Such a mechanism would be consistent with the slow evolution of motor neuron changes (chromatolysis) and the absence of excitotoxic damage in the frontal cortex of heavily dosed macaques exhibiting motorsystem (rather than convulsive) signs and the low levels of L-BMAA in the serum (micromolar) and cerebrospinal fluid (nanomolar) of one such animal [2,41]. Whether L-BMAA or its metabolite(s) target intracellular macromolecules critical for long-term maintenance of neuronal integrity is unknown.

L-BMAA is also metabolized to toxic species in rat tissue slices, mouse cortical explants, and rat crude cerebral microsomes. Nunn and Ponnusamy [42] reported that liver and kidney homogenates, but not brain homogenates, formed methylamine and 2,3-diaminopropanoic acid when incubated with L-BMAA. In contrast, Kisby and colleagues [43] found that rodent brain tissue metabolized both L-BMAA and aminopyrine (standard substrate for cytochrome P450) to the genotoxin formaldehyde, enzymatic reactions that were inhibited by the aminopyrine N-demethylase inhibitors deprenyl, SKF525A and piperonyl butoxide (Figure 5).

L-BMAA also interfered with brain RNA and protein synthesis when the amino acid was incubated with mouse cortical explants or administered intraperitoneally to adult rats (100 mg/kg) (Figure 6). In summary, while L-BMAA can act as a glutamate agonist, the amino acid is also taken up by brain tissue, forms a genotoxic metabolite, and regionally interferes with brain RNA and protein synthesis. These provocative findings suggest that further work on the non-excitotoxic properties of L-BMAA is merited, and it is premature to exclude the cycad amino acid as a participant in the etiology of western Pacific ALS-PDC.

2.2. Cycad Toxins: Azoxyglycosides and Methylazoxymethanol (MAM)

While further study of L-BMAA and its genotoxic metabolite in relation to ALS-PDC is encouraged, the results of our recent toxicogenomic studies have focused attention on a possible and perhaps more important etiologic role for MAM (Figure 7), the genotoxic metabolite of cycasin. Whereas cycads contain small concentrations of L-BMAA, cycasin—the glucoside of the potent DNA alkylating agent MAM—accounts for 4% w/w of Cycas seed [48]. Cycasin is thus delivered in much larger doses than L-BMAA when the raw seed is used as an oral tonic (Kii, Japan) or for wound repair (Guam, West Papua). Secondly, there is a striking correlation between the cycasin content of cycad flour and the historical age-adjusted incidence of both ALS and PD among both male and female villagers of Guam [49,50]. Third, MAM acetate is a developmental neurotoxicant that is used by the experimental neurobiologist as a reliable tool to disrupt regional brain development. Cycasin also induces cycadism, a neuromuscular disorder seen in large grazing animals (cows, goats) after ingestion of cycads [51]. Cycadism can be triggered by cycad plants containing various azoxyglycosides other than cycasin, all of which release MAM upon enzymatic hydrolysis [48] (Figure 7).

However, experimental studies that have tested the effects of cycad and components thereof on laboratory species are difficult to interpret. An early study [52] reported the development of an ALS-like disorder (unilateral arm weakness) in one of three monkeys fed Chamorro-style cycad flour, but another cancer-focused study with a larger number of animals treated with cycasin or MAM neither reported the neurological status nor examined the nervous system microscopically [53,54]. Studies of adult rodents have focused on the carcinogenic potential of cycad and cycasin, although cerebellar pathology was reported in a study of rats fed L-BMAA [55]. A recent experimental study of rats fed cycad materials (cycasin content unknown) found neuropathological changes in the substantia nigra, striatum, locus coeruleus and cingulate cortex [56] which, as the authors note, supports the proposed role of cycad in western Pacific ALS-PDC, a proposal first made by Whiting and Kurland, later resurrected by Spencer and colleagues, and now once again the subject of intense biomedical interest. Shaw and his colleagues, the authors of the recent rodent study, propose that cycad sitosterols—either as the free sterol or the glucoside—are likely etiological agents; this seems unlikely since these compounds are used to treat prostatic hypertrophy without reported neurological disease, and controlled toxicological studies have given these sterols a clean bill of health [57].

The word “synthesis” is defined as a combination of elements to form a connected whole. Thus, a synthesis essay definition is an essay that combines different ideas into a whole to prove a point (otherwise called the thesis). Often, it comes with a text that you should analyze.


Table Of Contents


Writing Process

A key factor of writing a synthesis essay is an analysis of a given text or a prompt. In order to successfully analyze it, you must comprehend the text’s purpose, rhetoric, and the argument that the author’s claim, in other words, you are answering the question: “So what?”. Then, you must build your own claim, and write an essay around that.

Most Common Topics

A synthesis essay prompt must be negotiable. Like in the EssayPro's example above, Andrew Jackson’s negative views on Native American people were widely supported, today, however, they would be appalling. Depending on your assignment, you may have to choose a primary text. Choose a text that might have opposing viewpoints.

Good topics would be ones that are debatable, for example:

  • Daylight savings
  • Minimum wage
  • Abortion
  • Immigration policy
  • Global warming
  • Gun control
  • Social media

How Do I Write A Thesis?

Once you pick a topic of your paper, read your sources and establish your position. Make sure you thoroughly analyze the sources and get a good understanding of them, structure your claim or argument and write your thesis.

Example: Andrew Jackson’s fear of the Native American “savages” reflects the prejudices and ideas of the colonist people in the Union and the Congress.*

How Do I Write An Outline?

Creating an outline will help maintain the structure of your paper. If your essay is split into three parts, split your outline into three chunks. Paste supporting evidence, sub-arguments, and specific points in the appropriate sections. Make sure that every point somehow proves the claim in your thesis. Extra information or tangents will only hinder your essay. However, if information goes against your central claim, then you should acknowledge it as it will make your essay stronger. Make sure you have read all of your sources. When writing about the sources, do not summarize them; synthesis denotes analysis, not plot-summary.

Example:

  • Introduction
  • Thesis
    • Main point 1
    • Main point 2
    • Main point 3
  • Body
  • Main point 1
    • Evidence (quote from a source)
    • Analysis of Evidence
  • Main point 2
    • Evidence (quote from a source)
    • Analysis of Evidence
  • Main point 3
    • Evidence (quote from a source)
    • Analysis of Evidence
  • Conclusion
  • Restate main points and answer unanswered questions

Read more about how to write a great INTRODUCTION

How Do I Format My Essay?

The format depends on what style is required by your teacher or professor. The most common formats are: MLA, APA, and Chicago style. APA is used by fields of Education, Psychology, and Science. MLA is used for citing Humanities, and Chicago style is used for Business, History, and Fine Arts. Purdue Owl is a format guide that focuses mainly on MLA and APA, and Easybib is a citation multitool for any of your external sources.

Some key points are:

  • Times New Roman 12 pt font double spaced
  • 1” margins
  • Top right includes last name and page number on every page
  • Titles are centered
  • The header should include your name, your professor’s name, course number and the date (dd/mm/yy)
  • The last page includes a Works Cited

APA Format

Some key points are:

  • Times New Roman 12 pt font double spaced 1” margins
  • Include a page header on the top of every page
  • Insert page number on the right
  • An essay should be divided into four parts: Title Page, Abstract, Main Body, and References.

How do I write an AP English Synthesis Essay?

AP English Language and Composition is an extremely rigorous course that requires you to write essays that demonstrate deep understanding of the subject matter. In fact, if on the AP exam, your essay has perfect grammar and structure, you might still be awarded just 1 out of 9 points for not “defending, challenging, or qualifying your claim.” Sounds difficult, but it is doable. Before entering any AP class, it is best to read over the course overview and become familiar with the exam.

While writing, focus on the three branches of the AP English and Composition course: argument, synthesis, and rhetorical analysis.

Argument is the easiest component; create your claim and find specific supporting evidence. Convince your reader that you are right.

Synthesis requires you to read into multiple perspectives and identify an agreement and a disagreement between sources. This step is crucial to finding your own claim.

Rhetorical analysis deals with the author and his intentions. What was their purpose for writing this? Who is their intended audience? How does the author appeal to the audience and how does he structure his claim?

Essay Tips

There are two acronyms that are helpful with the three AP Lang writing branches.

Tip #1: SOAPS

Example text: Andrew Jackson’s speech to the Congress about sending Native Americans to the West.

Speaker: Identify the speaker of the piece, then analyze for bias and apply any prior knowledge that you have on the speaker.

Example: President Andrew Jackson had a bias against Native Americans. A piece written by Andrew Jackson about Native Americans will probably be written with a bias against him.

Occasion: Determine the time and the place of the written text, then identify the reason the text was written. Even if you aren’t sure of the reason, assume one and make your claim around it.

Example: Andrew Jackson was in office from 1829 to 1837. At this time, the Congress sent Native Americans to the West in order to clear the land for the colonists. Jackson was the one who made the proposal.

Audience: Who was the text directed to?

Example: Andrew Jackson’s speech was directed to a council.

Purpose: What is the text trying to say? Here, you analyze the tone of the text.

Example: Andrew Jackson appeals to pathos by calling Indians “savages”. His purpose is to portray Native Americans in a negative light, so the Congress passes the Indian Removal Act.

Subject: What is the main idea? What is the claim?

Example: Andrew Jackson wants the Congress to pass the Indian Removal Act because he believes Native Americans are uncultured and savage people.

Tip #2: Logos, Ethos, and Pathos

As you’ve probably learned before, Logos appeals to reason, Pathos appeals to emotion, and Ethos appeals to moral philosophy or credibility. However, for the AP Lang exam requires a wider understanding of the three.

If the text uses facts, statistics, quotations, and definitions, the speaker is appealing to Logos. Constituting various backup information is an extremely effective for people who want to persuade.

If the text uses vivid imagery and strong language it denotes Pathos, which is used to connect the audience to a piece emotionally; it is hardest to change the mind of a person who is linked to a subject via a strong emotion.

If the text attempts to demonstrate the speakers reliability or credibility, it is a direct appeal to Ethos. Using the example above, Andrew Jackson could have appealed to Ethos by stating the fact that he is the President of the United States, and thus, knows what is best for the union.

Often, Logos, Ethos, and Pathos lead to the use of logical fallacies.

Tip #3: DIDLS

This is a good shorthand for all textual analysis. While reading a text, try to pinpoint Diction, Imagery, Details, Language, and Sentence Structure in a piece. If anything stands out, add it to your analysis.

Rubric

  • High range essay (8-9 points)
  • Effectively develops a position on the assigned topic.
  • Demonstrates full understanding of the sources or text.
  • Correctly synthesizes sources and develops a position. The writer drives the argument, not the sources.
  • The writer’s argument is convincing.
  • The writer makes no general assertions and cites specific evidence for each point. His/her evidence is developed and answers the “so what?” question.
  • The essay is clear, well-organized, and coherent. It is a stand alone piece rather than an exam response.
  • Contains very few grammatical and spelling errors or flaws, if any.

Note: 8-9 essays are an extreme rarity. A strong ‘7’ paper can jump to an 8-9 if the writing style is mature and perceptive.

Middle-Range Essay (57)

  • Adequately develops a position on the assigned topic.
  • Demonstrates sufficient understanding of the ideas developed in sources
  • Sufficiently summarizes the sources and assumes some control of the argument. ‘5’ essays are less focused than ‘6’ and ‘7’.
  • The writer's argument is sufficient but less developed.
  • Writer successfully synthesizes the sources and cites them.
  • Writer answers the “So what?” question but may use generalizations or assertions of universal truth. Writer cites own experience and specific evidence.
  • Essay is clear and well organized. ‘5’ essays less so.
  • Contains few minor errors of grammar or syntax.

Note: A ‘7’ is awarded to papers of college-level writing.
A ‘5’ on one of the AP English Language and Composition essays designates a 3 on the AP exam. It most likely relies on generalizations has limited control of the claim and argument. ‘5’ essays often lose focus and digress.

Low-Range Essays (1-4)

  • Inadequately develops a position on the assigned topic.
  • The author misunderstands and simplifies the ideas developed in the sources.
  • Over-summarizes the sources, lets the sources drive the argument.
  • Writer has weak control of organization and syntax. Essay contains numerous grammatical/spelling errors.
  • Writer does not cite the sources correctly, skips a citation, or cites fewer than the required minimum of the sources.
  • Notes: ‘4’ or ‘3’ essays do assert an argument but do not sufficiently develop it.
  • A ‘2’ essay does not develop an argument.
  • A 1-2 essay has severe writing errors and do not assert a claim.

Synthesis Essay Example

Essay Writing Advice From Our Professional Team

James Owen, online essay writer from EssayPro

The article reviews the basics of how to write a synthesis essay as well as how to dissect and analyze text when writing an AP English essay. One thing I would like to reemphasize is the importance of your thesis statement. When you write an essay for class or exam, make sure to state your argument clearly. If the reader of your essay doesn’t understand your point of view then what you’ve written is futile.

My advice is: when writing an essay in a short period (such as in an exam room) make sure to articulate your argument in every paragraph and connect every single one of your ideas to the thesis. My tip is to write your thesis down on a piece of paper and reread it at every point to ensure that the information applies and reinforces what you’ve stated in your thesis. This tip also goes for when you are writing a longer piece of writing, as it is very easy to lose focus and stray away from your main point.

Struggling With Writing an Essay?

Still having trouble crafting a synthesis essay? Need editing or writing help? You should seek advice from professional writers. Here at EssayPro, writers have written countless papers and are experts in their field. You can request to write your paper or editing or proofreading assistance. Rest assured that your paper is in good hands!

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