Respiration

Well I'm going to do some push ups when you are reading this, so why not join me! You see what happened there when you do a single push up? Your arms moved, your shoulders, your back and stomach moved. your heart pumped blood to all those different places. Pretty neat, huh? Well, it turns out that how we make and use energy is a lot like sports or other kinds of exercise. It can be hard work and a little complicated but if you do it right, it can come with some
tremendous payoffs. But unlike hitting a ball with a stick, it's so marvellously complicated and awesome that we're still unravelling the mysteries of how it all works. And it all starts with a marvellous molecule that is one of your best friends. ATP.

Today, I'm going to write about energy and the process our cells, and other animal cells, go through to provide themselves with power.

Cellular respiration is how we derive energy from the food we eat-specifically from glucose, since most of what we eat ends up as glucose. Here s the chemical formula for one molecule of glucose (C6H12O6). In order to turn this glucose to energy, we're going to need some oxygen. Six molecules of it, to be exact. Through cellular respiration, we're going to turn that glucose and oxygen into 6 molecules of C02, 6 molecules of water and some energy that we can use for doing all our push ups.

So that's all well and good, but here's the thing; we can't just that energy to run a marathon or something. First our bodies have to that energy into a really specific form of stored energy called ATP or adenosine triphosphate. People often refer to ATP as the "currency" of biological energy. Think of it as an pound sterling-it's what you need do business in the UK. You can't just walk into a book shop with a handful of Indian rupees and expect to be able to buy anything with them, even though they are technically money. Same goes with energy; in order to be able to use it, our cells need energy to be transferred into adenosine triphosphate to be able to grow, move, create electrical impulses in our nerves and brains. Everything.

Now, before we see how ATP is put together, let's look at how cells cash in on the energy that is stashed in there. Well, adenosine triphosphate is made up of an nitrogenous based called adenine with a sugar called ribose and three phosphate groups attached to it; now one thing you need to know about these 3 phosphate groups is that they are super uncomfortable sitting together in a row-like 3 kids on the bus who hate each other all sharing the same seat. So, because the phosphate groups are such terrible company for each other, ATP is able to do this nifty trick where it shoots one of the phosphates groups of the end of sit creating ADP, or adenosine diphosphate (because now there are just two kids sitting on the bus seat). In this situation, when the third jerk kid is kicked off the seat, energy is released. And since there are a lot of water molecules ust floating around nearby, an OH pairing- that's called a hydroxide-from some H2O comes over and takes the place of that third phosphate group. And everybody is much happier.

By the way? When you use water to break down a compound like this, its called hydrolysis- hydro from water and lysis from the Greek word for "separate." So now you know how ATP is spent, let's see how it's minted-nice and new-by cellular respiration.

Like I said, it all starts with oxygen and glucose. A lot of text books go on saying that through cellular respiration, one molecule of glucose can yield a bit of heat and 38 molecules of ATP. Now it's worth noting that this number is kind of a best case scenario. Usually it's more like 29-30 ATPs, ut whatever-people are still studying this stuff, so let's stick with that 38 number.

Now cellular respiration isn't something that just happens all at once-glucose is transformed into ATPs over 3 stages: glycolysis, the Krebs cycle, and the electron transport chain. Traditionally these stages are described as coming one after the other, but really everything in a cell is kinda happening all at the same time.

But let's start with the first step: glycolysis, or the breaking down of the glucose. Glycose, of course is a sugar-you know this because it's got an "ose" at the end of it. And glycolysis is just the breaking up of glycose's 6 carbon ring into two 3-carbon molecules called pyruvic acids or pyruvate molecules.

Now in order to explain how exactly, glycolysis works, I'd need about an hour of you time,  and a giant cast of finer puppets each playing a different enzyme, and through it would pain me to do it, I'd
have to use words like phosphoglucsosiomerase. But one simple way of explain it is this: if you wanna make money, you gotta spend money. Glycolysis needs the investment of 2 ATPs in order to work, and in the end it generates 4 ATPs, for a net profit, if you will, of 2ATPs. In addition, to those 4 ATPs, glycolysis also results into 2 pyruvates and 2 super-energy-rich morsels called NADH, which are sort of the love-children of a B vitamin called NAD+ pairing with energized electrons and hydrogen to create storehouses of energy that will later be tapped to make ATP.

To help us keep track of all the awesome stuff we're making here, let's keep score?

So far we've created 2 molecules of ATP and 2 molecules of NADH, which will be used to power more ATP production later.

Now, a word about oxygen. Like I mentioned, oxygen is necessary for the overall process of cellular respiration. But not every stage of it. Glycolysis, for example, can take place without oxygen, which makes it an anaerobic process. In the absence of the oxygen, the pyruvates formed through glycolysis get rerouted into a process called fermentation. If there's no oxygen in the cell, it needs more of the NAD+ to keep the glycolysis process going. So fermentation frees up to some NAD+, which happens to create some interesting by products. For instance, in some organisms, like yeasts, the product of fermentation is ethyl alcohol, which is the same thing as all of this stuff (alcohol). But likely for our day-to-day productivity, our muscles don't make alcohol when they don't get enough oxygen. If that were the case, working out would make us drunk, which actually would be pretty awesome, but instead of ethyl alcohol, they make lactic acid. Which is what makes you feel sore after
the workout that kicked your butt.

So your muscles used up all the oxygen they had, and they had to kick into anaerobic respiration in order to get the energy that they needed, and so you have all this lactic acid building up in your muscle tissue.

Back to the score. Now we've made 2 molecules of ATP through glycolysis, but your cells really need the oxygen in order to make the other 30-some molecules they need. This is because the next two stages of cellular respiration-the Krebs cycle and the electron transport chain, are both aerobic processes, which means they require oxygen.

And, so we find ourselves at the next step in cellular respiration after glycolsosis: the Krebs cycle. So, while glycolysis occurs in the cytoplasm, or the fluid medium within the cell that all organelles hang out in. the kerbs cycle happens across the inner membrane of the mitochondria, which are generally considered the power centers of the cell. The krebs cycle takes the products  of glycolysis-those carbon rich pyruvates-and reworks them to create another 2 ATPs per glucose molecule, plus some energy in a couple of another forms, which i'll talk about in a minute.

Here's how: first, one of the pyruvates is oxidized, which basically means it' combined with oxygen. One of the carbons off the three-carbon chain bonds with an oxygen molecule and leaves the cell as CO2. What's left is a two carbon compound called acetyl coenzyme A, or acetyl coA. Then another NAD+ comes along, picks up a hydrogen and becomes NADH. So our two pyruvates create another 2 molecules of NADH to be used later. As in glycolysis, and really all life, enzymes are essential here; they are proteins that bring together the stuff that needs to react with each other, and they bring it together in just the right way. These enzymes bring together a phosopahte with ADP, to create another ATP molecule for each pyruvate. Enzymes also help join the acetyl coA and a 4-carbon molecule called oxaloacetic acid. Together they form 6-carbon molecule called citric acid which is in orange juice.

Fun fact; the krebs cycle is also known as the citric acid cycle because of this very byproduct. But it's usally referred to by the name of the man who figured it all out: Hans Krebs, an ear nose throat surgeon who fled Nazi Germany to teach biochemistry at Cambridge, where he discovered this incredibly complex cycle in 1937. For being such a total freaking genius, he was awared the Nobel Prize in Medicine in 1953.

Anyway, the citric acid is then oxidized over a bunch of intricate steps, cutting carbons of left and right, to eventually get back to oxaloacetic acid, which is what makes the krebs cycle a cycle. And as the carbons get cleaved off the citric acid, there are leftovers in the forms of CO2 or carbon dioxide, which are exhaled by the cell, and eventually by you. You and I, as we continue our existence as people, are exhaling the products of the krebs cycle right now. Good work.

Now, each time a carbon comes off the citric acid, some energy is made, but it's not ATP. It's stored in a whole different kind of molecular package. This where we go back to NAD+ and its sort of colleague FAD. NAD+ and FAD are both chummy little enzymes that are related to B vitamins, derivatives of Niacin and Riboflavin, which you might have seen in the vitamin aisle. These B vitamins are good at holding on to high energy electrons and keeping that energy until it can get released later in the electron transport chain. In fact, they're so good at it that they show up in a lot those high energy-vitamin poweders for the kids are taking these days.

NAD+S and FADs are little batteries, big awkward batteries that pick up hydrogen and energized electrons rom each pyruvate, which in effect charges them up. The addition of hydrogen turn them into NADH and FADH2, respectively. Each pyruvate yields 3 NADHs and 1 FADH2 per cycle, and since each glucose has been broken down ito two pyruvate, that means each glucose molecule can produce 6 NADHs and 2 FADH2s.

The main purpose of the krebs cycle is to make these powerhouses for the next and final step, the Electron Transport Chain.

And now's the time, when you are saying "Sweet pyruvate sandwhiches, Rebekah, aren't we supposed to be making ATP? Let' make it happen. capt'n What's the holdup?" Well friends, your patience had paid off, because when it comes to ATPs, the electron transport chain is the real moneymaker. In a very efficient cell, it can net a whopping 34 ATPs.

So remember all those NADH's and FADH2s we made in the krebs cycle? Well, their electrons are going to provide the energy that will work as a pump along a chain of channel proteins acorss the inner membrane of the mitochondria where the krebs cycle occurred. These proteins will swap these electrons to send hydrogen protons from the inside the very center of the mitochondria, across its inner membrane to the outer compartment of the mitochondria. But once they're out, the protons wantto get to the outer side of the inner membrane, because there's a lot of other protons out there, and as we've learned, nature always tends to seek a nice, peaceful balance on either side of a membrane. So all of these anxious protons are allowed back through a special protein called ATP synthase. And the energy of the this proton flow drives this crazy spinning mechanism that squeezes some ADP and some phosphates together to form ATP.

So, the electrons from the 10 NADHs that came out of the krebs cycle have just enough energy to produce roughy 3 ATPS each. And we can't forget our friends the FADH2. We have two of them and they make 2 ATPs each. And volia! This is how animal cells thhe world over make ATP through cellular respiration.

Now just to check, let's rest out ATP counter and do the math for a single glucose molecule once again. We made 2 ATPs for each pyruvate during glycolysis. We made 2 in the krebs cycle. And then in during the electron transport chain we made about 34 in the electron transport chain, And that's just for one molecule of glucose. Imagine how much you body makes and uses every single day.

Don't spent it all in one place now!

Is inheritance really all in our genes?

We can inherit a lot from our parents. Hair and eye colour, height. But we can't inherit everything, because some biological traits are acquired during our lifetime. The only way to transmit biological information between generations is the letters of our DNA. But what if its not simple? What if our environment, and our experiences can be passed on to our children and grandchildren? Inheritance is turning out to be much weirder than we think.

Every cell in your body holds an incredible 6 feet (1.8m) of DNA. The same 6 feet of DNA, each holding identical genetic instructions. Yet when skin cells regenerate every day, the new ones somehow "know" to become skin cells, not bone, or muscle. Something beyond DNA influences their destiny. This is what scientists call epigenetics differences in traits that aren't due to changes in the DNA sequence. When it's wrapped up inside the cell, tiny chemical flags on the DNA or the proteins it's coiled around signal the cell to turn certain genes on or off, so they make just the right machinery to do their job. These chemical flags rewritten every day as organisms adapt to new environments, but scientists are seeing something strange: some of these changes can be passed on to the next generation.

Mice fed high-fat diets.. get fat (unsurprisingly) thanks to changes in the chemical flags on their DNA. But female children of these obese mice, even though they were taken away and were raised by normal mothers still ended up 20% fatter than mice from skinny parents. In another example, male mice trained to dear a fruity odour passed sensitivity to this smell on to their children and grandchildren. even thought their offspring had never been exposed to it.

If this sounds a lot like what that guy Lamarck was talking about, well you're not wrong. Before Darwin, may scientists thought acquired traits could be passed on, but natural selection proved that wrong.

But even so, scientists have since seen cases in species from flowers to fruit flies where traits are passed on to children and grandchildren without changing the DNA sequence.

Thre's jus one catch. This shouldn't be possible.

Just hours after an embryo's is conceived, its chemical flags are erased, so all the cell types in the new body can be built from a blank slate. And cells destined to become sperm and eggs get erased a second time. At leasts that's what scientists thought. For epigenetic inheritance to work, some flags must sneak through without being reset. This strange inheritance might even happen in human. During the Dutch famine at the end of WW11, children undernourished in the womb still carried epigenetic changes more than 60 years later. And sicne these changes happen in the womb, they could have a huge effect on our health as adutls.

In Overkalix, Swwden, boys who lived through good harvests had sons and grandsons with higher rates of diabetes and heart disease while boys who lived through winter famines had healthier grandsons-they lived an average 32 years. Strangely, gilrs who lived through swings of feats and famine had granddaughters with higher rates of heart disease.

That is confusing. But human lives aren't easily-controlled lab studies and that's why some scientists doubt this new kind of inhertience.

Epigentic changes can definitely happen between one or two generations, but for a trait to have an effect on evoluation, it had to endure for dozens of generations.

When a baby's developing, the cells that will make a grandchild are aleady present, and can be exposed to do the same environment as the grandmother. That's not inheritance as much as super-duer early exposure. For epigenetic changes to be truly inherited, they have to be rewritten un every generation, we'd have to see them in great-grandchildren and beyond, and that's just not clear yet,

Even so, the vast majority of triats that make us who we are written in our DNA and it's tough to totally rule out genetic changes or other factors even in the cases we've seen. That's the problem with studying complex animals whose lives are the product of thousands of genes in trillions of cells. There's a lot going on here.

But since many of our diseases are linked to stress, diet, or environement, it wouldn't be totally surprising to find out our bodies are affected in ways we didn't know about.

Epigenetics is a young science, and it's reminding us we have a lot of learn about what makes us who we are.

Lewy body

We're back at Dementia station, today you are going to learn about Lewy body dementia.

Lewy bodies dementia is named after microscopic changes in the brain, which differentiate from all other types of dementia. In the UK, it is thought that 10,000 suffer from dementia with Lewy bodies at the moment of time there is 700,000 people with this type of dementia and the number is only going in increase unless a cure is found.

Dementia with lewy bodies is a type of dementia that shares symptoms with Alzheimer's disease and Parkinson's disease. Dementia with lewy bodies can be mistaken as other conditions.

Causes

Lewy bodies dementia is causes by an abnormal amount of protein called lewy bodies inside brain cells. These are also found in people with Parkinson's disease so they are similar to each other. They disrupt the brains normal function and interfere with the chemical signals that are passed from one brain cell to another. Lewy body dementia usually occurs in people that have no history of the condition, even though there have been rare cases that lewy body been inherited from family.

Lewy bodies are tiny bits of protein in the nerve cells. They are linked to low levels of chemical messages and a loss of connections between the nerve cells. Overtime, the nerve cells die and there is a loss of brain tissue.

Signs and symptoms

Like other types of dementia, the condition cause symptoms of thinking speed, language, understanding, judgement and memory. However, significant memory loss may not occur until later on. A person with lewy body dementia might display a symptom of extreme swings between alertness and confusion or drownnissness, which can change unexpectedly from hour to hour to day to day. Furthermore, they might have slow movements, get stiff limbs this will cause a person shuffle when they are walking. A person with lewy body dementia might experience hallucinations where they hear or see things are not actually real and can range from being pleasant to distressing.

Lewy bodies can also be found in the brains of people Parkinson’s disease, and so people with this type of dementia often have a number of symptoms that affect their movement.

Someone with lewy body dementia may experience fluctuating consciousness. This is where a person experience large swings in levels of confusion. Some days the confusion is extreme and are unable to function whereas other people could follow the plot of a film or play a game of cards pretty decently these fluctuations can also happen minute by minute or hour by hour.

Around two thirds of people with lewy body dementia experience visual hallucinations (seeing things that aren’t there but are visual that they seem real). People who experience hallucinations commonly see animals these can  be quite pleasant for some people, but frightening hallucinations can be pleasantly distressing.

Spontaneous parkinsonism produces the usual symptoms of Parkinson’s disease, such as muscle stiffness, slow movement, tremor, shakiness and less of facial expressions.

Someone with lewy body dementia may experience visuospatial difficulties. The start of the dementia can be heralded by increasing clumsiness. As people are robbed of their ability to judge widths and distances falls and breakages are common, as are bumps (or worse)when parking or driving a car.

The thought processing (cognitive symptoms) of dementia are all those of loss. People with lewy body dementia with, to one degree or another, lose their memory, their judgement and quite literally their way.

Another symptom that a person with lewy body dementia may experience sleep disorders, a person might be able to sleep easily during the day, but are restless and disturbed at night because of rapid eye movement where the person tries to act nightmares. This can be very distressing or can be physically harmful for partners.

Physical aggression can be direct result of changes in the brain caused by dementia, or side effacers from medication that is prescribed to treat the dementia. Paranoid delusion and hallucinations can also prompt protectively aggressive reactions. Equally, though aggression can be caused by things that would annoy anyone but that generate a more extreme reaction as a result of the disinhibitions that can occur due to changes in the brain. These other triggers include; noisy surroundings, pain, hunger, thirst, and the person simply not getting on with someone.

Effects

 

People with lewy body dementia are at a higher risk of falls. Especially in the later stages a person may experience a worsening, movement problem which means that when a person walks they get slower and less steady. This means falls become more common.

Eventually someone with lewy body dementia is likely to need intensive nursing care. This can make the person feel they are loosening their home and unable to look after themselves.

During the later stage of dementia a person with lewy body dementia may experience problems with day-to-day memory which is very similar to those people with Alzheimer’s in the middle or later stage. This would affect the individual ability to remember the common words for things which can lead to frustration and confusion, even anger. Furthermore, this can make a conversation an extreme trail.

A person with dementia may lose they identity because no on would include them in the conversation. No one would adapt the way they say things which can make someone with lewy body dementia feel excluded or isolated.

If a person can’t comprehend what has been said, this person might need more time more to process the information unfortunately their relatives don’t allow their loved ones enough time to process the information. In fact they rush there loved  which can make this individual become frustrated, People can also become frustrated if they can’t find the answer to a question which means they could respond back with irritation or even aggression.

 

Chemicals from Oil

Next stop is chemistry, today you would have a guided tour about chemicals from oil.

How oil is formed?

Natural gas is formed alongside of oil and it is thought that oil was formed of millions of years from the break down of tiny dead creatures.

Dead organisms sank to the bottom of lakes or seas and become trapped in muddy sediments. As the sediments build up, the lower layers were under pressure. They returned to rock. If there were no oxygen in the sediments, heat and pressure turned the remains of the organisms into oil and natural gas.

Some rocks are porous-they have a network of tiny holes in them such as sandstone. Oil is liquid so it seeps into porous rocks. Gas also diffuses into these rocks.

Porous rocks may also contain water. Gas and oil do not mix with water. They are less dense than water which means they form layers above the water.

Sometimes the rock layers form so that oil and gas are trapped under the rock such as shale that is not porous. Large amounts of oil and gas may collect in a porous rock. The pressure on the oil may build up so much that when a hole is drilled through the rock cap, oil gushes out.

Fractional distillation of crude oil

Crude oil is a mixture of many thousands of different compounds with different properties. They are called hydrocarbons because they only contain the elements hydrogen and carbon.

To make crude oil useful, batches of similar compounds with similar properties needed to be sorted. These batches are called fractions and they are separated by fractional distillation.

The theory behind this technique is that some of the compounds in crude oil are easily vaporised, for example they are volatile due to their low boiling points. Others are less volatile and have higher boiling points.

In fractional distillation, the crude oil is heated to make it vaporise. The vapour is then cooled. Different fractions of the oil are collected at different temperatures.

As the hydrocarbon molecule chain increases its boiling point increases, it becomes more viscous, becomes more difficult to light, the flame becomes sootier and it develops a stronger smell.

BBC (2006) GCSE Bitesize: Alkanes. Available at: http://www.bbc.co.uk/schools/gcsebitesize/science/aqa/crudeoil/crudeoilrev1.shtml (Accessed: 8 April 2016).

Frontotemporal dementia

First train station is dementia. Here you would you have a guided tour about dementia. Today you would be learning about a dementia called frontotemporal dementia.

Frontotemporal dementia (FTD) is relatively rare among forms of dementia, it is sometimes called pick disease or frontal lobe dementia. Furthermore it affects around 16,000 people in the UK.

Frontontemporal dementia occurs much less than other forms of dementia such as Alzhimer's disease or Vascualr dementia. However it is significant cause of dementia in younger people who are under the age of 65 which makes Frontontemporal dementia  the third most common cause for people. In this age brackets it affects men and women equally. Frontontemporal dementia  is most often diagnosed between aged 45-65 though it can affect younger or older people in this considerably younger than the age at which people are most often diagnosed with dementia such as Alzheimer's disease.

The word Frontontemporal dementia  refers to the frontal and temporal lobes that are the regions of the brain that are impaired this form of dementia. The frontal lobe function is thinking, planning, organizing, problem solving, inhibitions, personality and emotions. The temporal lobe function is the memory and processing the language.

There are four types of Frontontemporal dementia. Firsly, behavioural variant Frontontemporal dementia  influnces somone behaviour and cause an individual to not socialize with another appropriately. Secondly, primary progressive aphasia which refers to impairment in language ability this would influence someone ability to communicate and process it. Thirdly, progressive suprancuclear palsy this affects someone balance, cognitive and movement. Someone with this type of frontotemporal dementia will notice they would have a impaired eye moment. Finally, the corticobasal degeneration appears as muscle weakness and tremors and usually affects only one side of the body. As the disorder progress, a person may experience memory and behavior symptoms.

Causes

There are many causes of Frontotemporal dementia, but they can all involve a build-up of abnormal tau proteins in the brain. The abnormal proteins clump together and because toxic to brain cells, which eventually kills them and that causes the affected areas of the brain to shrink over time. We do not fully know why these abnormal proteins build up, but research has found a genetic component, up to 40% of people with Frontotemporal dementia inherited if from their family. Also lifestyle factors can also cause Frontotemporal dementia.

The mutated gene that can affect Frontotemporal dementia are MAPT, GRN or C90RF72 which all play a part in how proteins work n the body. Children of those who carry the gene are at 50% risk of inheriting it.

Signs and symptoms

Symptoms of frontotemporal dementia usually develop gradually and increasing worse over a number of years. Many people will either have behavioural or language problems. As the condition progress, most people experience problems in both of these areas as well as additional physical problems and thinking difficulties. Eventually, the condition spreads to affect most brain functions.

First several years a person with frontotemporal dementia may experience dementia mild.

At this stage, main symptom is mostly behavioural changes such as disinhibition can make someone to make inappropriate comment or at it socially unacceptable ways. Someone might lose the empathy and sympathy they may not show any understanding or be able to show forgiveness to someone. Later on they may developed 'obsessional' behaviours that can include repeating the same words over and over again and hoarding items. Also a person might experience difficulty planning and organizing and sometimes memory. They know a something is wrong but can't put a finger on it, over the contray they can still be capable of managing household tasks and self-care with minimal help.

A person may show reduced inititative and lack of personal hygiene, becomes easily distracted or repeat the same action repeatedly; this is where overeacting or compulsively putting objects in the mouth may occur.

A person with frontotemporal dementia may experience the ability to communicate in expressive speech so they cannot express themselves and receptive speech which is the ability to understand speech. As I said before someone may have trouble finding the right word, speak very slowly, when they read or write they find it incredialy difficuly and not be able to form sentences in a way that make sense to them and other people.

Someone with frontotemporal dementia might display motor actions or the ability to control movement. They may have unwanted arm and leg movments or shakiness consequently they may fall frequently. Intresting fact, a person's memory and understanding of the space around them often remain intact especially in the earlier stages.

Effects

A person with impairment in judgement can lead to financial indiscretion which can lead to catastrophic consequences such as

Someone with frontotemporal dementia  might withdraw themselves away from their friends and relatives. Sometimes an individual might behave inappropriately with strangers, lose their social manners, act spontaneously Sometimes people with frontotemporal dementia  break laws because they loosed their inhibitions. At this stage, the behaviours can often be managed with lifestyle and environmental changes. A MRI image at this point will show mild atrophy in particular areas of frontal lobe.

If someone worked a shop it would affect them because since they not able to give sympathy and empathy towards a customer or even understand their perspectives of the problem. This may lead to the shops loose their customers or an individual is unable to do her/his job which means they would find themselves in a financial problem or rely their family to take in. This would also mean the family would get a closer to their relatives.

A person with frontotemporal dementia  might have a psychological effect like lack of motivation because a person may become very passive such as siting in front of the television or appear to lose interest in hobbies such as reading and when you say to a person with frontotemporal dementia "let's read a chapter of Wuthering Heights." They may give a big sigh because for them to read it takes a lot of effort for them and they got no motivation to read.

A person might not be their usual self in ways that are difficult to identify or even to explain. A person may becomes depressed or anxious in situations where memory problems are causing difficulties.

Websites I used

Heerema, E. (2016) Frontotemporal dementia symptoms, types, treatments. Available at: http://alzheimers.about.com/od/typesofdementia/a/What-Is-Frontotemporal-Dementia.htm (Accessed: 7 April 2016).

Symptoms1 (2013) Available at: http://www.dementia.com/symptoms.html (Accessed: 7 April 2016).

Want any more information about dementia then this website is really good (haven't used as such, just looked at it without writing notes.)  http://www.uniassignment.com/essay-samples/health/difference-between-dementia-and-alzheimers-disease-health-essay.php

Aboard on the train

Welcome my passengers. Anyone need a ticket who has just come aboard from Brillant Becca Bakes?

Right so why have I set up a new blog when I already have a personal blog. Basically I attend college I go to lecture's just like normal college students. I write notes from the  PowerPoints, read textbooks and of course research the internet. Come to my assignments I forget what I was learning about it is like you are doing coursework but haven't learned anything.

I love writing and telling my friends what I learned about. So I thought why not start posting my lecture notes and tips for me on my blog. Then I realized there was a problem, not many people might want to read my lecture notes on my other blog. It just won't fit the style of that blog. I will set up a new blog that would make lecture notes fit which is this new fantastic blog.

Since you are reading this you might wonder what type of things I will write about. At the moment I am going to write up my assignments on here. Hopefully by doing this it won't be called plagiarized since it is my own blog. But hey it is worth a try. Then when I got my assignments out of the way, I would be typing up my lecture notes and gather any information from my textbook and of course the internet. I will be referencing the resources which might be helpful if you do health and social care.

Now you would be starting to think, what if I don't do health and social care? Well I am more likely to post different things on here like Maths and creative writing. Plus you are here not to learn like school but just for enjoyment.

Whatever your reason for stumbling over this blog, you are going to have a fun journey on the train each station you would have different knowledge.