Alzheimer’s disease (AD) is the most common form of dimentia, a disease characterised by severe memory loss, mood changes and communication problems. AD is a progressive disease which gets worse overtime. Patients suffering with rapidly degenerative AD eventually require full-time care as they become unable to complete day-to-day tasks, such as cleaning and cooking.

AD was first reported by German neuropathologist Alois Alzheimer in 1906 when he identified abnormal clumps of proteins called amyloid deposits in the brain of a woman who had suffered with strange behavioural symptoms, including severe memory loss . This later became the basis for the amyloid plaque hypothesis of AD, however how these plaques cause AD remains unknown (1).

With the latest statistics revealing that over 820,000 people are currently living with AD in the UK and one person being diagnosed every 3.2 minutes, the requirement for effective early diagnostics tests and curable treatment is becoming increasingly urgent (2). One in three people aged over 65 will die with a form of dementia. Dementia costs the UK approximately £23 billion per year. Caring for each person with dementia has an economic impact of £27,647 per year, which is 4.6 times greater than the figure for cancer.

Etiology

To date, despite intense research efforts, there is no identified single cause of Alzheimer’s disease. However, several factors have been demonstrated to play a part in increasing the risk of AD. The first is age. Statistics revel that 1 in 14 over 65 year olds and 1 in 6 over 80-year-old suffer with AD. The second factor is genetic inheritance. Although the majority of cases are sporadic, 0.1% of cases are familial forms of AD, meaning that risk genes may be passed on through families. Other studies have linked the risk of AD with other factors, including head injury, tobacco smoking and lack of exercise (3).

Management

Although Alzheimer’s disease remains an incurable disease, management is available, but remains only able to treat certain symptoms in the aim of improving the quality of life of AD sufferers. There are three branches of management available, including drugs, care giving and psychological treatment. A total of 5 drugs have been approved for treatment towards AD. Four of the approved drugs are acetylcholinesterase inhibitors, these include Tacrine, Rivastigmine, Galantamine and Donzepil. These drugs are recommended based on the hypothesis that AD patients brains reveal a loss of nerve cells that send messengers through the hormone acetylcholine. These drugs break down acetylcholine to improve symptom severity. The fifth drug is an glutamate blocker called Memantine. This drug is prescribed based on the theory that AD brains release excessive amounts of the messenger, glutamate. Memantine blocks these effects. Efficacy, however, is patient-specific (4).

Diagnosis

At present, the diagnosis for Alzheimer’s remains a combination of different tests, including patient and family history, clinical observations, such as neurological and neuropsychological features, memory tests, and the absence of other conditions. Brain imaging is becoming an increasingly useful examination for Alzheimer’s.

Positron emission tomography (PET) is a neuroimaging tool which is used in combination with memory tests as part of the diagnostic methods for AD.  PET imaging is used based on the hypothesis that areas of high brain activity are associated with high radioactivity. As it has been demonstrated that glucose levels are greatly decreased in AD brains, a measurement of glucose is able to distinguish AD from other types of dimentia (5).

News: Alzheimer’s test approved

On the 6th April, the FDA approved Amyvid (a Florbetapir F18 Injection) a new drug for PET 3D imaging of the brain for adults being evaluated for AD. In this method the compound florbetapir binds to amyloid plaques and is detected by PET imaging (6,7).

Currently, a reagent called Pittsburgh Compound B is used to image amyloid plaques in people suspected to have Alzheimer’s disease. However, as this compound is labelled with carbon-11, which has a half-life of just 20 minutes. Therefore, its use is limited. Another more useful chemical florbetapir is labelled with fluorine-18, which has a half-life of nearly two hours. Thus, long enough would be long enough to be used in the brain and be imaged without losing too much dye. Not only will imaging with florbetapir be able to reveal the development of amyloid plaques in AD brains, but it will also be able to demonstrate the relationship between amyloid plaques and AD, in order to work towards a cure.

Reactions

There is, however, controversy surrounding the approval of this drug and it’s use in a diagnostic test. As reported in a Blog by Nature, although scientists were initially hopeful for the potential of Amyvid in the AD diagnosis; autopsies of AD brains have demonstrated that one-fifth of suspected AD patients did not have amyloid plaques. Therefore, the diagnosis was wrong. It is important to acknowledge that amyloid plaques alone are not solely indicative of AD. Additionally, other forms of dimentia also present with amyloid plaques in the brain. As the underlying mechanisms of the amyloid hypothesis and its involvement in AD have not been fully elucidated, further research is required (8).

Therefore, although the approval of this test could be a step toward determining the pathology of AD and producing a diagnosis test, we are a long way from a fully elusive testing procedure. With this in mind, possible patients need to decide whether they wish to undergo a test, that may produce a false-positive result that may change their lives forever.

References

(1) http://alzheimers.org.uk/site/scripts/documents_info.php?documentID=100

(2) http://www.alzheimersshow.co.uk/the-statistics/

(3) http://www.medpagetoday.com/Neurology/AlzheimersDisease/32088

( 4) http://alzheimers.org.uk/site/scripts/documents_info.php?documentID=147

(5) http://www.webmd.com/a-to-z-guides/positron-emission-tomography

(6) http://blogs.nature.com/news/2012/04/alzheimers-diagnostic-probe-approved.html

(7) https://investor.lilly.com/releasedetail2.cfm?ReleaseID=662647

(8) http://www.medpagetoday.com/Neurology/AlzheimersDisease/32088

Avian flu (bird flu) is a highly contagious virus that infects  a wide variety of birds, causing a varying state of disease. Symptoms observed in infected birds are similar to those caused by influenza in humans. There are over 26 types of avian flu virus, but the deadliest strain to date is the infamous H5N1. According to WHO, there have been 583 recorded cases of H5N1 infection in humans, occurring in countries such as Turkey, Vietnam and China, which have led to a total of 334 deaths; over half of all infected. Controversy has arisen among scientific groups as to whether research demonstrating the mutations that cause this deadly virus to infect mammals should be published for everyone to access. With headlines such as ‘Bird flu terrorism over study’s publication’ hitting the media, the impact of this story that will shape the future of engineered virus research.

The papers

At the end of last year, two research papers were submitted to the journals Nature and Science. The first paper was a study conducted by Ron Fouchier and his team at the Erasmus Medical Centre in Rotterdam, The Netherlands. In their study, the team passed a mutant H5N1 virus, with three mutations, two in the HA surface protein and one in the polymerase enzyme, known to allow bird flu to infect mammals, through ferrets. The virus strain killed the ferrets subjected to the virus, but the virus did not transmit between ferrets in different cages. Then, the team passed the virus from the already infected ferrets through healthy ferrets 10 times and the virus picked up new different mutations. After the 10th passage, the virus spread to ferrets in separate cages through aerosol transmission and killed them. Two new mutations were observed in all viruses in the dead ferrets, which added to the three incorporated mutations disclosed five key mutations. Fouchier concluded therefore that upon passage, the virus had collected mutations that enabled the virus to spread through ferrets, but are they the only mammals the virus could spread to?

Following recommendations from the USA’s National Science Advisory Board for Biosecurity (NSABB), the authors were asked to redact key details of the papers, The board released a statement on 20th December stating that although research on the H5N1 strain has public heath benefits, it also has ‘ potential to be misused for harmful purposes’. Therefore, they recommended the publication of the papers with the deletion of methodology, so that the research could not be repeated, but anyone including other researchers; this did not go down with the science community.

The two journals ‘grudgingly’ agreed to publish redacted versions without details of methods or mutations, despite opinions that for the best interest of public health the information needed to remain accessible. In return however, the Government promised to develop and implement a system by which scientists could access the papers, however, information on how and who will be allowed access was not provided.

Editor-in-chief of Science Bruce Alberts said ‘many scientists within the influenza community have a bona fide need to know the details of this research in order to protect the public, especially if they currently are working with related strains of the virus’.

Should the studies have been conducted?

However, controversy has arisen over whether the research should have been conducted in the first place. On the one hand, the research could lead to screening systems for detected strains of the virus, which aim to identify key mutations which make the virus transmissible. The studies could also lead to increased research and the development of vaccines for the flu, similar to what was achieved for swine flu.

On the other hand, certain opinions believe that the laboraories who conduced the experiments and engineered the viruses could have put the public at risk of danger. Not only becuase the virus could have leaked out from the lab, infecting susceptibles which could have lead to a pandemic, but because the study demonstrates to anyone how the deadly virus could be made, which could be used as a weapon. The lab-created version, the board warned, represented an “extremely serious global public health threat”. These points alone demonstrate the seriousness of this work.

At the end of December, WHO said limiting access to the research cannot be achieved as it would be impossible to decide who should get access and who shouldn’t. WHO also said that it would be impossible to stop publication. A meeting regarding the future of the studies was planned for February and in the meantime a 60-day ban on all research on H5N1 was allowed; this was agreed upon by the two journals.

The verdict

Following the meeting in February, this system still has not been devised. In fact, WHO have no concluded that it could take years to develop. Instead following the meeting WHO advised the studies should be published in full, but not immediately. 

This week

On the 29th February, it was announced that the NSABB were to be given redacted versions of the two papers, for a second round of review. At the present time, no date has been given for this.

References

http://news.sciencemag.org/scienceinsider/2011/12/grudgingly-virologists-agree-to.html

http://www.bbc.co.uk/news/world-us-canada-16279365

http://www.upmc-biosecurity.org/website/resources/publications/2011/2011-12-15-editorial-engineering-H5N1

http://www.nih.gov/news/health/dec2011/od-20.htm

http://www.newscientist.com/article/mg21128314.600-five-easy-mutations-to-make-bird-flu-a-lethal-pandemic.html

http://www.nature.com/nature/journal/vaop/ncurrent/full/481443a.html

http://www.ctv.ca/CTVNews/Health/20120229/panel-bird-flu-studies-120229/

http://www.iol.co.za/scitech/science/news/mutant-virus-not-as-lethal-as-previously-thought-1.1246320

Parkinson's disease symptoms

Parkinson’s disease is a progressive neurodegenerative condition which affects the central nervous system. The disease is caused by a lack of dopamine-producing cells in the substantia nigra region of the brain. Without sufficient dopamine, movement are slow, giving rise to the common motor symptoms including tremor, bradykinesia (slowness of movement), rigidity and postural instability, and the neuropsychiatric symptoms including, executive dysfunciton, memory loss and depression (1).

Statistics from the Parkinson’s UK website report that 1 in 500 people have Parkinson’s disease, which is equivalent to approximately 127,000 people in the UK. Although the majority of these people are over 50 years old, 1 in 20 are under 40 (1).

The breakthrough

On the 7th February, a paper entitled ‘Parkin controls dopamine utilization in human midbrain dopaminergic neurons derived from induced pluripotent stem cells’ by Jiang et al was published in Nature Communications. The paper reported the successful creation of human brain cells that are exact replicas of cells in Parkinson’s disease. The study was based on the hypothesis that a type of Parkinson’s disease can be caused by mutations in genes such as parkin.

In the study, Jiang and his team for the first time were are able to generate pluripotent stem cells from normal subjects and PD patients with mutations in parkin. Pluripotent stem cells are able to develop into different types of cells, for example skin, blood, brain and bone, by a process known as differentiation. They are self-renewal and have the potential to be used in treatment to repair and renew mutated or deficient cells to treat diseases. These stem cells were transformed into brain cells that are seen in patients with mutations in parkin. This remarkable step, is the first time that scientists have been able to artificially reproduce these cells, in order to examine the mutations that cause the Parkinson phenotype, meaning that the exact mutations that cause the disease can now be fully investigated,

The study demonstrated that loss of the parkin gene, increased the transcription of monoamine oxidases and oxidative stress, significantly reduced the uptake of dopamine, and increased the spontaneous release of dopamine. The scientists used expression of lentivirus to insert the parkin gene to demonstrate that parkin controls dopamine levels in the brain and enhances its transmission. Therefore, indicating new targets for treatment and diagnosis. If scientists are able to develop a clinical method of inserting normal parkin into mutated cells, they might me able to prevent this type of Parkinson’s disease from occurring (2).

The future of treatment

The work from this study could be the key to developing future personalised treatments, which target mutations in parkin. They study also opens the door to studying the brains complex circuitry and pathways.

This accomplishment, Feng says, is advancing not only the study of Parkinson’s but other neurological diseases simply by enabling researchers to non-invasively study the disease at its cellular level. “It finally allowed us to obtain the material we needed to study the disease” (3).

Dr Feng said “This is the first time that human dopamine neurons have ever been generated from Parkinson’s disease patients with parkin mutations. Before this, we didn’t even think about being able to study the disease in human neurons. The brain is so fully integrated – it’s impossible to obtain live human neurons to study”.

Dr Michelle Gardner, Research Development Manager at Parkinson’s UK, concluded that “New stem cell technology which allows nerve cells to be made from adult skin cells is opening doors for research into Parkinson’s”.

This is an exciting and optimistic time for Parkinson’s researchers and patients, as a step is taken toward treatment for this currently incurable disease (3).

References

(1) http://www.parkinsons.org.uk/about_us/news/news_items/all_news/nerve_cells_parkin_gene.aspx:

(2) http://www.nature.com/ncomms/journal/v3/n2/full/ncomms1669.html

(3) http://www.bbc.co.uk/news/health-16913997

In the last few weeks, it has been reported that 1 in 4 toddlers are lacking in vitamin D (1). This has lead to one case of rickets a month in hospitals causing experts to believe that daily recommendations on vitamin D supplementation are not being followed (2). According to a study, nearly three-quarters of parents and more than half of health professionals are unaware of the recommendations. This comes after the shocking case of the death of baby Jayden Wray, whose parents last month were acquitted of his murder, following medical reports that Jayden was suffering from rickets, which could be to blame for the complications which lead to his death. With this highlighted case and others being discovered now, it is now vital  that awareness regarding the importance of vitamin D supplements is increased, to decrease the number of cases of rickets and prevents headlines such as those seen in the figure below.

What is rickets?

Rickets is a disease that affects children that is caused by weakening and softening of the bones. The weight of the upper torso puts intense pressure onto the leg bones, which causes them to bow or change shape and in severe cases even break. Rickets gets its name from the Old English word “wricken” meaning twisted. This disease in adults is called osteomalacia.

During the 1600s, rickets was epidemic in England due to reduced sunlight caused by smog and smoke. The cause of rickets was not identified until the 1920′s when the Government issued a public health programme advising children received plentiful milk, vitamin D and calcium. This lead to the near eradication of rickets in the UK and other industrialized countries. In the 1950′s, rickets cases began to fall and with it so did awareness of vitamin D.

The most common type of rickets is nutritional rickets and occurs due to deficiency of vitamin D, calcium and phosphate.

Vitamin D

Vitamin D is a group of fat-solube secosteroids similar to steroids, but with a broken ring. It is required for the absorption of calcium in the  gut. Without enough calcium, bones deformities can occur. Vitamin D is found in a variety of common dietary foods, including oily fish, eggs, cereals and milk. However, vitamin D requires conversion from its inactive state to its active state. This is conducted by UV light in the sun. The capacity to convert 7-dehydrocholesterol in keratinocytes into vitamin D (calciferol) depends on exposure to ultraviolet B rays. Therefore, the prevention of rickets requires sufficient dietary vitamin D and sufficient sunlight. Vitamin D is synthesized in the body, and therefore is not actually a vitamin, but a prohormone.

Signs and symptoms

Common symptoms of rickets include:

• soft skull bones
• delayed closing of the soft spot at the top of a baby’s head
• poor growth
• floppy limbs and body due to muscle disease or weakness
• teeth taking longer to come through
• weak tooth enamel that may lead to tooth decay
• bone pain in the arms, legs, spine and pelvis
• fractures (3).

Diagnosis

If rickets is suspected in a child, x-rays are taken to examine for features of rickets in the bones such as  bowing, fractures and shape abnormalities (as shown in the image above). Following x-ray examination, the cause of rickets can be determined by blood tests which measure levels of calcium, phosphorous and vitamin D.

Prevention and treatment

The incidence of vitamin D deficiency is rising worldwide, yet in the vast majority of patients, the condition remains undiagnosed and untreated. Public health recommendations imposed by the Government advise vitamin D supplements. It has been clinically proven that vitamin D doses greater than 800 IU/day have beneficial effects on the musculoskeletal system, improving skeletal homeostasis, thus leading to fewer falls and fractures.

Most people can get all the vitamin D required through eating a balanced diet and getting a little sun. Vitamin D is easily accessible in foods such as oily fish, eggs and milk. However, the Department of Health recommends a daily vitamin D supplement for the following people:

• all children aged six months to five years
• all pregnant and breastfeeding women
• all people aged 65 and over
• people who aren’t exposed to much sun, for example people who cover up their skin for cultural reasons, or people who are housebound (stay indoors) for long periods of time
• people with darker skin, such as people of African-Caribbean and South Asian origin

Why is rickets making a come back?

The main reason that the number of cases of rickets is increasing is because public awareness regarding of vitamin D has fallen. If parents are not educated as to the importance of vitamin D for their children then can unintentionally put their children at risk of deficiency. Yet if the information needs to get to parents in the first place. Ultimately, then it is the role of Doctors, midwives and health care assistants to educate parents. Once this is established, then lifestyle changes can be made.

In order to maintain a healthy balanced life, children need to establish a balance between spending  time outside in the fresh air getting exercise and maintaining a healthy, balanced diet. Due to warnings about the rick of skin cancer, the public are over cautious in the sun and excessively cover up their skin, preventing their body from accessing sufficient vitamin D. However, a little sun is healthy and can protect against rickets.

I hope by writing this article, I am doing my bit towards increasing awareness of the importance of vitamin D and the risk of rickets.

References

(1) http://www.mirror.co.uk/news/health-news/2012/01/25/rickets-returns-as-1-in-4-toddlers-found-to-be-lacking-in-vitamin-d-115875-23718769/

(2) http://www.bbc.co.uk/news/health-16700833

(3) http://www.bbc.co.uk/news/uk-england-16107085

(4) http://www.bupa.co.uk/individuals/health-information/directory/r/rickets#textBlock259205

If you have found this article interesting, please answer the poll below.

A study conducted by a team including Maria Ohlsson Teague and Dr Michelle Lane at the University of Adelaide, Australia has produced interesting results which may demonstrate one example of a genetic process by which obesity is passed on to offspring in mice.

In the study, mice were screened for changes in DNA that caused proteins to be switched off. It was demonstrated that in male mice that were fed a high fat diet, 21 proteins were expressed differently. Upon examination of the proteins that had altered expression, it was revealed that these proteins were involved with sperm development and metabolic disorders. These then led to the production off unhealthy offspring.

These results show one example of the importance of a healthy diet. It is suggested that eating habits cause changes in chemicals which interact and modify DNA, which affect gene activity and protein production. These changes are called ”epigenetic” and occur when sperm are exposed to environment or lifestyle-related factors which have impact on reproductive function and may be passed onto subsequent generations. While this theory has long been hypothesised, this is one of the first studies that has demonstrated marked evidence.

In conclusion, the researchers showed not only that obese male mice produced unhealthy offspring, but a possible mechanism behind why this happened. The results from this finding, if proven to be supported by other studies, could lead to the development of screening systems which examine sperm for such epigenetic changes. This could further lead to the production of drugs which can be used to prevent these changes. However, that time is a long way off. For now this study demonstrates the significance of healthy lifestyles not only for the benefit of the individual , but for the benefit of future generations.

Reference

http://www.newscientist.com/article/mg21228434.900-highfat-diet-leaves-its-mark-on-sperm.html

Influenza viruses are part of the Orthomyxoviridae family, and are divided into 3 genera; influenzavirus A, B and C. Types A and B are the most common, therefore only these will be discussed. Members of the type A species of influenza include the strains H1N1, which caused the swine flu epidemic in 2009, and H5N1, which caused the bird flu pandemic in 2004. Type B strains almost only infect humans, are less common, mutate 2-3 times slower and are less genetically diverse, therefore pandemics of influenza B cannot occur.

The most effective way to protect against influenza is by vaccination. Vaccines for influenza have been available since the 1950′s, and are capable of preventing 70-90% of illness. Despite the World Health Organisation vaccination recommending flu vaccination, the proportion of vaccine uptake in the UK remains low.

The advantages of the vaccine is that it is highly protective, free if you are in the at-risk group and easily accessible. However, unlike other vaccine in which one injection in most cases while keep an individual protected for their lifetime, a  new influenza vaccine is available every year from September onwards. This is because every year there is a new influenza strain that circulates and becomes dominant, so protection needs to be adjusted accordingly. Influenza epidemics can vary in their timing, severity, length and virus strain, meaning that it is highly unpredictable; this needs to be taken into consideration when designing a new vaccine.

How is a new flu vaccine produced each year?

A new flu vaccine is required to be produced each year due to the virus’ nature of constantly changing. Every winter different strains of flu circulate, meaning that while the symptoms of flu might be similar, it could actually be a different virus that it causing the infection.

In order to prepare for this, action must be taken months in advance of the winter season. Therefore, in February of every year, WHO have to make an assessment of the flu strains that are most likely to be circulating in the northern hemisphere in winter. They do this by continually surveying the pattern of influenza infections through the Global Influenza Surveillance Network (GISN) and through information from advisers from international institutions and laboratories. As well as infection patterns, WHO have to consider the evolving strains of flu virus and strains of influenza virus that have caused sporadic infection, such as avian and swine strains which can cause infections in humans and lead to a pandemic. Influenza strains are also continually assessed for resistance to anti-viral drugs, so that evaluations of the effectiveness of therapeutics can be conducted.

Following this assessment, the three most likely strains are selected for the vaccine. This year the three strains that WHO have recommended to be protected against  in the 2011-2012 season in the northern hemisphere are:

• An A/California/7/2009 (H1N1)-like virus
• An A/Perth/16/2009 (H3N2)-like virus
• A B/Brisbane/60/2008-like virus

Flu vaccine production and accessibility

The vaccine is manufactured by growing the three selected strains in hen’s eggs. The viruses are then killed and purified and made into a vaccine. As the virus strains are killed, and the virus is not live, it is not possible to develop flu from the vaccine. The flu jabs are available from local GP surgeries, Boots drug stores and are even now offered to your office by a company run by the Fleet Street Clinic, London.

Conclusion

In summary, flu is a highly infectious disease which can be prevented through vaccination. As it is a virus, antibiotics are not effective and therefore vaccination is the main protection. Individuals in the at-risk group are highly advised to have the vaccination to prevent the severe diseases that can occur from influenza infection. Individuals not in the at-risk group can pay privately for the vaccination; the immune systems of these individuals should be strong enough to fight of influenza protection within one week.

Finally, may I ask everyone to take an extra minute to look at the link below and sign up for the FluSurvey. This is an independent flu infection tracking website, which measures flu trends in the UK directly from the general public, with the aim of gaining more accurate information on flu epidemics in order to predict and prevent them. See website: http://flusurvey.org.uk/en/

References

http://www.flujabs.org

http://cancerhelp.cancerresearchuk.org/about-cancer/cancer-questions/should-i-have-the-flu-vaccine

http://www.hpa.org.uk/web/HPAweb&HPAwebStandard/HPAweb_C/1222154877315

What do you know about the flu jab? Should you be getting it? Why do we need it? Look out for an informative post at the end of this week.

As last Thursday 1^st December was World AIDS day, I thought it was appropriate this week to give a short update on news concerning AIDS and HIV. Unfortunately, the news is mixed as the ongoing battle against this devastating disease continues.

Last week saw the release of a report from the United Nations that revealed the most encouraging statistics on AIDS to date. The number of new infective cases have fallen markedly through the successful implementation of drugs that prevent the infective transmission of the disease. However, the achievement of the therapies could soon come to a halt as reports from the UN have exposed that funding targets recently have not been met. Countries including Italy and Spain have not paid towards the scheme for the last two years. As a devastating result, operations are having to be scaled down meaning that current research projects and treatment programmes will not be able to continue to make the progress they currently are. A report from WHO and Unicef has revealed that after a steady increase in funding, last year funding for HIV programmes fell from $8.7bn to $7.6bn.

Also reported this week was the news of encouraging experiments in mice and monkeys which suggest that a non-traditional approach to a vaccine for HIV might be the way forward. The hypothesis behind this new vaccine is to target not the immune system but muscles. The hope is that injections of genes into the muscles which produce factories which pump out antibodies against HIV.

David Baltimore and his team at the California Institute of Technology loaded a stripped down virus called adeno-aassociated virus (AAV,) which produces a mild cold infection, with genes that when expressed produce antibodies to HIV. The viruses were injected into leg muscles and the results were examined.  It was demonstrated that the mice produced antibodies against HIV and remained healthy even upon infection with HIV, which revealed that the gene therapy was successful.

Whilst this hypothesis sounds promising and mouse models had to date demonstrated efficacy, , the effect in humans however will not be known until clinical trials. Baltimore’s team has said that the technique will not be available for testing in humans for year or two. Even if the therapy reaches that stage, then the vaccine could still fail at several stages. A similar approach demonstrated in macaques by Johnson et al in Philadelphia revealed positive results, so researchers are hopeful that the same results will be seen in humans.