Breakthrough in Neurodegenrative disease!

Today many of you may have heard about the discovery of the first chemical to prevent the death of brain tissue in neurodegenerative disease. That’s right…scientists have discovered a chemical which has been able to prevent brain cell death in mice. Although more work is needed to develop a drug that can be consumed by a patients this is a turning point in the fight against Alzheimer’s, Parkinson’s, Huntington’s and other diseases.

Yes, it is true that many problems can occur on the road from drug for a mice to a drug for a humans. But, this is the first time that a chemical has been discovered to COMPLETELY halt neuro-degeneration which would suggest that this process has a lot of potential. Even though neurodegenerative disease all progress in a different way researches in this case are targeting the way in which the cell deals with the protein misfoldes this means that one drug can become the cure for many diseases!!!

The study, which was published in Science Translational Medicine , showed mice with the disease developed severe memory and movement problems. They died within 12 weeks. However, those given the compound showed no sign of brain tissue wasting away.

Yes there is still a long way until we are able to develop a cure for neurodegenerative diseases but this discovery is big step on the road to finding that cure.

Hepatitis C Virus

Hepatitis C virus (HCV) causes chronic inflammation in the liver of humans which can lead to cirrhosis or even liver cancer. The virus is able to get inside cells and make new copies of its genetic material using the machinery of the host cell. The new viral DNA is then packaged into new partials and leaves the cell to infect other cells. Some people have an immune system which is able to clear the virus easily, however, for most of us it develops into a lifelong infection. Although, it is possible to get a liver transplant when it no longer works this is only a short term solution, as the transplanted liver becomes re-infected.


Transmission of HCV requires blood to blood contact.  In addition any source of blood or blood products seems to be capable of carrying the virus, even if the source is indirect – like a used razor. Once effective blood screening techniques were developed and used in 1990 post transfusion hepatitis rates decreased from about 8-10% to 5% between 1990-1993. And improved testing methods led drastic reductions in risk (less than 1% after 1993). Needle-stick injuries, contaminated medical equipment, and blood spills in health care settings are also responsible for many cases of HCV. Drug use, however, is the most significant risk for contracting HCV. Sharing contaminated needles increases your chances for developing the infection drastically.


Not everyone experiences symptoms for HCV in the first few months. But some make experience the following symptoms in the first six months (this stage is called acute hepatitis C.):

  • a high temperature of 38C (100.4F) or above
  • tiredness
  • loss of appetite
  • stomach pains
  • Nausea

For some people  the immune systems gets rid of the virus successfully so they experiences no more symptoms but for the remaining cases the virus may persist for years. At this point it is known as chronic hepatitis. Some people still don’t experience any symptoms but for some it can have a significant impact on their lives.

Treating hepatitis C 

Majority of HCV cases go untreated as symptoms aren’t visible or not experienced.

Treatment for chronic hepatitis C usually involves using a combination of two medications:

  • pegylated interferon (an injection) – a synthetic version of a naturally occurring protein in the body that stimulates the immune system to attack virus cells.
  • ribavirin (given as a capsule or tablet) – a type of antiviral drug that stops hepatitis C from spreading inside the body.

The effectiveness of these medications is dependent on the genotype of the HCV. Genotype 1 is more challenging to treat. Only half of people treated with combination therapy will be cured.

Other genotypes respond better to treatment, with a cure rate of around 75–80%.

Genetic Diversity in HCV

Viruses tend to mutate quickly. HCV has a short genome of about 10,000 nucleotides. Unlike human cells Viruses don’t have a proofreading mechanism which can correct mistakes in replications, therefore, when the virus replicates the incorrect nucleotides are retained. Additionally, HCV has a high replication rate. Both these factors mean that a large number of mutations can accumulate over a time. This allows the virus to avoid the immune response if the host, as the changes occur in regions of the genome that eh cells is programmed to recognise.

HCV sample of infected people in different parts of the world can differ by up to 30%. This suggests that there a great amount of genetic diversity in this species. The high rate of mutation makes it difficult to develop a vaccine for the virus as vaccines target specific components of the virus but if this changes the vaccine becomes ineffective.


Hepatitis C is divided into six distinct genotypes with multiple subtypes in each genotype class (classification of a virus based on the genetic material in the RNA strands of the virus. Genotype 1 is the most common type of Hepatitis C genotype in the United States but can also be found in Africa, Europe and japan. However, it is endemic in Africa but epidemic in the Europe and the USA. Genotype 1 is also the hardest to treat with about 50% success rate whereas genotype 2 and 3 have a higher success rate of about 80%.

New drugs for the treatment of hepatitis C are now being investigated in phase II and phase III clinical trials. These include interferon-sparing regimens, which are needed for the treatment of those intolerant to, or medically ineligible for pegylated interferon and ribavirin therapy. New drugs are also targeting viral enzymes to prevent the viral life cycle to complete.


Double-jointedness (joint hyper laxity/hypermobility) is a medical condition which affects approximately 3% of the population.

A contributing factor to joint hypermobility is a person’s genetic instructions for making the protein collagen which may cause the collagen to form so that it is relatively weak and this will mean that ligaments are more easily stretched, and thus the joints are more flexible.

Joint hypermobility can also be caused by more serious conditions such as Ehlers-Danlos Syndrome Vascular Type (EDS IV) and Osteogenesis imperfecta. These have potentially serious complications.

Hypermobility has a few advantages for example:

  • It can be very useful in some sports. E.g. in cricket: bowlers with long, thin, flexible fingers are likely to be able to produce better spin on the ball when they bowl.
  • Music is another example-playing the piano or guitar would be much easier if you were to have hypermobile fingers.

But of course there are also some disadvantages:

  • Lack of understanding of the condition can itself have an emotional influence on those with it. Many suffer from frustration, anger and even depression.
  • Joint pain particularly during growth spurts in females.
  • More likely to endure painful injuries such as dislocation, fractures, ligament sprains, muscle strains and so forth.



What Is Pain?

Pain can be described as a sensation with causes discomfort, and perhaps agony. It may be constant or a throbbing pain.

Pain which originates from the nervous system is called non-nociceptive because there are no specific pain receptors. Nociceptive means responding to pain. When a nerve is injured it becomes unstable thus its signalling system becomes muddled. The brain interprets these abnormal signals as pain. This randomness can also cause other sensations, such as numbness, pins and needles and tingling. As a result pain can sometimes be unpredictable.

Types of pain

One type of pain is acute pain; this is a short lived (up to 30 days) but intense pain (also known as acute pain). This tends to indicate some form of injury, hence when the injury heals the pain ceases too. Another type of pain is Chronic pain, which lasts longer than acute pain (duration of more than six months) but can be mild or intense.

How do we classify pain?

Nociceptive pain– in this case there is a stimulation of peripheral nerve fibres. Receptors here detect temperature (heat/cold), mechanical activities (crushing/tearing) and chemical activities (chilli powder in eyes).
Deep somatic Pain – This is a type of nociceptive pain. Somatic pain (muscular-skeletal pain) is the name given to pain which can be felt on the skin, muscle, joints, bones and ligaments. This type of pain tends to be aching, poorly localized pain. An example would be sprained ankles.

Superficial pain- this is initiated by activation of nociceptors in the skin or other superficial tissue. These receptors are capable of sensing inflammation, stretch and ischemia. It tends to be located in internal organs and main body cavities, such as thorax (lungs and heart), abdomen (bowels, spleen, liver and kidneys), and the pelvis (ovaries, bladder, and the womb.)


Neuropathic Pain- This is a type of non-nociceptive pain. The pain can originate from the peripheral nervous system or the central nervous system. It may be caused by nerve degeneration in cases such as stroke and multiple-sclerosis or it may have been caused due to a trapped nerve (there is pressure on the nerve).  A slipped disc will cause nerve inflammation, which will trigger neuropathic pain as will a nerve infection, for example shingles.


Sympathetic Pain- this type of pain tends to occurs after a fracture. This pain is non-nociceptive hence there are no specific pain receptors. As with neuropathic pain, the nerve is injured, becomes unstable and so the brain receives abnormal, which it interprets as pain.

Phantom Pain- this involves the sensation of pain in a part of the body that has been removed.  Though no one knows for sure why amputees have phantom pain there are possible explanations which are widely accepted.

  • Memory of limb pain – some researchers theorise that brain had become accustomed to the pain when the limb was badly damaged. So even when the limb has been removed, the brain continues to sense the same kind of pain
  • Nerve bundle stimulation – Others suggests that nerves around the amputation are stimulated in some way, sending signals to the brain which it interprets these as pain.
  • Rewiring of the nervous system – there has also been evidence to show that that when a limb is amputated, changes take place in the brain and spinal cord which may mean that  pain is interpreted differently however it is not clear if this causes phantom pains.


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