Neurodegeneration – a common cure?

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By Dr Laura Phipps | Wednesday 09 October 2013

Today’s papers are reporting a ‘potential breakthrough’ in treating all neurodegenerative disorders. Surely this sounds too good to be true? Let’s look in a bit more detail at the concept behind this research…

What do neurodegenerative diseases have in common?

The term ‘neurodegenerative disease’ covers a whole span of conditions, all resulting in the loss of nerve cells and gradual decline in the ability of the brain to keep going:

  • Alzheimer’s is a very common neurodegenerative disease, affecting around half a million people in the UK
  • Parkinson’s, which affects 127,000 people in the UK
  • Huntington’s disease, affecting more than 6,000 people
  • There are also rarer neurodegenerative diseases like Creutzfeldt-Jakob disease (CJD).


Alzheimer’s disease is characterised by an abnormal build up of two proteins – amyloid and tau.

In Alzheimer’s disease, the culprits are two proteins called amyloid and tau. In Parkinson’s (and dementia with Lewy bodies), it’s a protein called alpha-synuclein. In Huntington’s the Huntingtin protein cause the problems and in diseases like CJD, it’s a protein called prion.

Taking a step back

While it’s incredibly important to understand the detail of, and differences between, each of these diseases, it’s also worth standing back and looking at them all as a whole. Is there a mechanism common to more than one neurodegenerative disease? Could we develop a treatment that stops all these proteins from clumping together, irrespective of their differences?

This is exactly what scientists at the Medical Research Council (MRC) Toxicology Unit at the University of Leicester are suggesting this week. We first reported on findings from this team back in 2012, when they looked at the effect on cells of the prion protein, which is involved in diseases like CJD.

They showed that the build-up of abnormally folded prion protein triggers a defence response in cells which temporarily shuts down protein production. This makes logical sense – if something is going wrong, stop it first and find a way to fix it.

But the team believes that in prion disease, and possibly in other neurodegenerative diseases too, this protective response becomes damaging. They have shown that it shuts down for too long, preventing the cell from making other proteins vital for survival.

In this most recent study, the researchers used a compound designed to reactivate protein production in cells and found that it could slow neurodegeneration in mice with prion disease and protect them from memory and thinking problems. Whether this holds true in people with prion disease, or is relevant to other neurodegenerative disease such as Alzheimer’s, still remains to be investigated. But it’s an interesting proof-of-principle study and a potentially important finding.

What is Alzheimer’s Research UK doing?

Today’s research suggests that perhaps we should be careful not to lose sight of the woods for the trees. Investigating each of these diseases individually is vital, as it allows us to:

  • Characterise each disease
  • Help people understand and manage their symptoms
  • Improve diagnosis
  • Look for treatments specifically suited to people with that disease.

But we should also look at what these diseases have in common.

And that’s something we’ve addressed at Alzheimer’s Research UK in our new Research Strategy. We’ve identified some important questions that still need to be answered. These include investigating mechanisms common to all of these neurodegenerative diseases:

  • How do nerve cells die in response to these abnormal proteins?
  • How do these proteins spread across the brain?

We hope that by funding research in these areas, as well as all the research we support looking at each of these diseases in their own right, we can help science make progress for even more people affected by these cruel diseases.

See also:


  1. RufusG on 10th October 2013 at 6:30 am

    Alzheimer’s can be stopped today.
    Based on 35 years research at Oxford University:

    Read more at:

  2. Rockin Ron on 10th October 2013 at 10:24 am

    Well done to Prof. Mallucci and her team at University of Leicester. Was this funded by Alzheimer’s Research UK? Hope this proves to be a turning point and goes on to give hope to many people.

  3. Ian Viney on 10th October 2013 at 11:01 am

    Professor Mallucci is funded by the Medical Research Council (MRC), previously at the MRC Prion Unit at UCL and now at the MRC Toxicology Unit at Leicester University details at

  4. MJHopeC on 10th October 2013 at 4:11 pm

    Presented here at AD/PD 2009: 9th International Conference on Alzheimer’s(AD) and Parkinson’s Diseases (PD), Murray Waldman, MD, from St. John’s Rehabilitation Hospital, in Toronto, Ontario, found that while citations in the medical literature for femur fractures rose from 1706 to 3730 between 1996 and 2000, citations for AD and other dementias shot up from 1274 to 21 569 during the same time period.

    This dramatic spike over 40 or so years, he said, cannot be accounted for by an aging population, “because what we were looking at was incidence, not prevalence.”

    Epidemiological data collected over a 25-year period shows the incidence of AD in the 1960s was 2% in people over the age of 85 years, whereas today, most experts accept that the incidence of AD in this population is 50%. It is 20% over the age of 75 years and 10% in individuals over the age of 65 years, he added.

    “So the incidence seems to have soared enormously in this brief period.”

    Briefly that this is due to a metabolic (cellular) switch resulting in “misfolded” proteins that cause neurones to die. This raises three questions:

    1) What caused the “switch” as this seems to have occurred in the last 70 years or so because before that the incidence of AD was very low. (The claim that this is due to improved diagnosis seems debatable as the first people to identify dementia are family and friends).

    2) If the “switch” is natural, what caused it? Was it drugs, diet or infection? Surely identification of the cause of the switch is more important than finding a drug to “cure”?

    3) Would such a “cure” be a one-off or a life time treatment? An important question for pharmaceutical profit.

    • duckbita on 10th October 2013 at 5:23 pm

      A cogent comment, one thing strikes me …

      ” 2) If the “switch” is natural, what caused it? Was it drugs, diet or
      infection? Surely identification of the cause of the switch is more
      important than finding a drug to “cure”? ”

      Both prevention and cure are worth pursuing. Prevention research is funded by public money, cure is really Pharma’s “business”. Epidemiology is surely one of our most powerful tools?

      • MJHopeC on 11th October 2013 at 9:59 am

        Read Dr James LeFanu’s Book “The Rise and Fall of Modern Medicine” The Social Theory section.  Having been trained at the LSH&TM when Prof. Bradford-Hill was there and been  working on  epidemiological subjects for much of  my  working life, epidemiology is indeed as use guide but it largely only identifies associations not causality; the results have to be internally coherent.  As it is currently being  used, it depends on what is put in which is not necessarily relevant; there are too many inconsistencies resulting from this misuse, even abuse. It is a quick way to get answer to one’s liking.

  5. Rupert Bowling on 13th January 2017 at 7:11 pm

    That would be fantastic if there was a breakthrough.

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Dr Laura Phipps