A little bit of hope on a lovely spring day

Not being able to retrieve memories is one of the many cruel symptoms of dementia.  I have written a short memoir about the poignant moment when my mum, in the early stages of the condition, told me that she’d cried herself to sleep the night before because she couldn’t remember her life.

The notion of a scientific breakthrough to provide treatments enabling those with Alzheimer’s disease (by far the most common form of dementia) to rediscover their lost memories is a powerful one.   Now a new study has done just that – in mice.  Because I don’t like articles that give false hope I’m going to say, right here at the top of the story, that four out of five breakthroughs that show promise in studies with mice fail when they are tested on people.

And yet the accounts I’ve heard and read of this latest study are interesting enough to warrant a blog, so here it is.  A little bit of hope for a spring day.

On Radio 4’s Today programme, which you can listen to here, the study’s supervisor, Professor Susumu Tonegawa of the Massachusetts Institute of Technology described how, working with mice who had been specially bred to have the early stages of Alzheimer’s, his team discovered that the mice had not lost the ability to make memory, but the ability to retrieve stored memory.  “Using technology called optogenetics basically we cured this impairment in the mice,” he said.  (Optogentics is, put very unscientifically, the use of light to control cells in living tissue).

It was this aspect – that the team were able to “tease out the different types of memory deficit that one can see in Alzheimer’s disease” – that Dr Simon Ridley, Director of Research at Alzheimer’s Research UK, found so “interesting and exciting”; though he warned on the same Today programme that the study was of the earliest changes in the disease.  In later stages, when someone has suffered significant nerve cell loss and symptoms have become more apparent, the reversal is probably less likely.

As he outlined a possible early stage case study where the breakthrough information might apply – his language laced with caution and caveats – he provided as good an explanation of the disease itself, and of its difference from the normal effects of ageing, as I’ve heard in some time.

It’s worth quoting in full.  “What we believe happens –we still don’t know all the details – is that in Alzheimer’s disease, certain proteins start to build up, one of which is amyloid.  Over time, amyloid builds up, the connections between the nerve cells – which are crucial for normal brain and neuronal function – become irreversibly damaged and the brain cells die.  Other things happen: the brain develops a phenomenon called neuro-inflammation in which inflammatory cells are activated.  There’s a vicious circle of damage that ultimately results in a person dying – over two decades perhaps”.

An important part of Dr Ridley’s explanation is that the damage and ultimate death of the brain cells can result in the individual dying.  Alzheimer’s disease, the most common form of dementia, ultimately results in dying.   According to the Office for National Statistics, in 2014 the leading cause of death in women in England and Wales was dementia; it was the third most common form of death for males.  So many people I talk to (outside the knowledgeable “dementia community” of those with a personal or professional connection to the condition) are unaware of this.

And as if to underscore this, Dr Ridley stated in no uncertain terms that age-related memory decline, which doesn’t impact on people in a significant way, was quite different – “ a different beast” as he graphically put it – from Alzheimer’s disease.  It is so good for an authority to state this categorically on prime time radio.

Overall, I’d say Dr Ridley’s reaction to the news of a breakthrough in memory retrieval was cautious excitement.  He was quite clear that the “contrived but very clever system of optogenetics” used by Professor Tonegawa’s team was “very, very unlikely to ever be useful in humans.  But he was optimistic that in the long-term such nerve damage in humans could be reversed – through “different routes”.

“What one is looking at,” he said, “is strategies to understand and hopefully repair the damaged connections in the early stages before it is too late”.

I respect the research director’s caution.  I applaud the extraordinary scientific breakthrough of the team led by Nobel prize winner Professor Tonegawa, a man the Times lauded as “a master of memory” in its leader column.  And I agree with the leader writer who concluded, “We can only wait and hope.  In the meantime, the researchers should be congratulated on another remarkable display of the power of fundamental science to answer questions the rest of the world had never thought to ask”.  I am grateful that this time the question they sought to answer was on a subject so close to my heart.