Review: Misterman

 

Misterman (at the National Theatre until 28 May) starts sweetly enough. Cillian Murphy (star of Solar, 28 Days Later) rattles manically round a disused warehouse which is decked out with strip lighting, bare bulbs, junk. Doris Day sings “Everybody Loves a Lover,” creamily soft, like a pat of butter. There’s a bit of physical comedy: he can’t turn the tape off!

OK, maybe this man-child is just a little too exuberant. Whoa - and really sloppy with his props. Violent, even. Things get thrown about the place; later, as Misterman Thomas Magill reenacts conversations with his fellow townsfolk, there’s an unhinged carelessness to the way he pours tea, which splashes over furniture and floor.

Writer Enda Walsh takes your Irish dinky pastoral and smashes it to bits. The smithereens mosaic into something altogether harder and harsher. In your face, Ballykissangel.

This garage-space is full of reel-to-reel tapes (Beckett fans will note the debt to Krapp’s Last Tape), which Thomas uses to play the other half of conversations and the FX of daily life, and especially a barking dog, recorded in his hometown of Innisfree. He cues in the sounds and voices, corrects himself (sometimes the tape corrects him). The show that Thomas is putting on is clearly a long time in rehearsal. We gradually understand that he will be rehearsing these scenes, which all relate to a single day, for a long time to come. The debris filling the garage could be the jumble in his own head: areas (like the cluster of crucifixes) light up as though neural pathways have been activated.

The populace of Innisfree (Murphy broadens his accents and acting style to do “types”) are a banal and self-interested lot, who struggle to talk of anything beyond the commonplace. With that special Irish ear for the surreally comic in the everyday, Walsh has them make statements like, “there’s a great honesty to the milk of magnesia".

Murphy’s voice has the piping squeak of a breaking one; his clothes are ill-fitting and filthy. The film star jawline and head have sprouted hair - just those charged blue eyes laser right to the back of the stalls. He’s tested to his limits in impersonating the town’s inhabitants, and miming encounters with them. He has fights with invisible assailants, or uses props for people: unnervingly his “Mammy,” whose back he’s massaging with Vick’s, is a table. His is a performance that burns with zeal.

Thomas, who is “touched” (but not necessarily by the divine), senses that there is something beyond all this. He has visions, walks with angels, feels God’s immanence. He’s God’s conduit and recording angel, with a tape deck slung round his neck. One neighbour shows “immodesty". Another is “indecent". “Fuck you and your fucking words,” says one, to Thomas. But his own language is as restricted as theirs: it’s a schoolboy catechism that he spouts, and a pollyanna Garden of Eden he seeks, where apples “pop into life".

From Genesis we hurtle to Revelations, and from recording to avenging angel. His brutal encounter with the Roger the dog - the tale could have been rewritten as The Curious Incident of the Dog in the Daytime - prefigures a still more savage act of retribution. The soundscape collapses in on itself - Doris Day’s buttered tones surface again, then are supplanted by a mangled Toploader (“Dancing in the Moonlight”) at the local community centre dance.

Here Thomas straps on a pair of wings, spits bile at the townsfolk/us, and confesses his dark deeds from the gantry. Murphy takes his lunacy up a notch.

Misterman’s not easy listening, or watching. There are periods where an andante lyricism stalls to largo. At others it’s a little like being repeatedly lashed with rosary beads. The play’s perhaps too fixed on inter-textual chat with Beckett and Yeats to speak very clearly to us. It also places enormous stress on Cillian Murphy, the lone performer; a lesser man would have lost us. 

 

Cillian Murphy in Misterman. Credit: Catherine Ashmore
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The best defence against Alzheimer’s

Spoiler: the best way to avoid Alzheimer's is to stay young.

At the recent meeting of the European Academy of Neurology in Copenhagen, doctors were signing up to attend a workshop teaching non-specialists to test for cognitive decline in their patients. How do you tell the difference between a scatterbrain and a case of early dementia?

It’s a question that is increasingly urgent. Last year, 47.5 million people were living with dementia. That will have risen to 75.6 million by 2030 and will reach 140 million in 2050. The World Health Organisation has declared that dementia should be regarded as a global public health priority. But what can we do about it?

The primary cause of dementia, accounting for roughly 70 per cent of cases, is Alzheimer’s disease. It’s all very well to put a name to it, but we don’t have a clear understanding of the mechanisms that cause it – or medicines to battle it. Alzheimer’s drugs have a high rate of failure. In the decade to 2012, 99.6 per cent of newly developed drugs failed to make it past clinical trials. There is no cure for Alzheimer’s and none on the horizon, either.

There was, however, a small breakthrough last month. A study published in the journal Science Translational Medicine suggests that Alzheimer’s could be a result of fighting infections from other diseases that would, if left unchecked, ravage the brain. The hard lumps of sticky plaque in the brain that characterise the onset of Alzheimer’s seem to be the result of the immune system attempting to isolate and neutralise microbes and other pathogens that have made their way into the brain. The plaques catch pathogens, preventing infection from taking hold. Unfortunately, it’s a case of damned if you do, damned if you don’t: the plaques also trigger inflammation that leads to the death of brain cells.

This observation mirrors another catch-22 with Alzheimer’s. Some researchers have suggested that the drug failures might be averted by getting candidate treatments to the disease earlier, before symptoms appear. Put simply, the drugs may stand a better chance of success when trying to counter the first stages of damage to the brain. The problem is: how do you get that early diagnosis?

There are various genetic indicators for a heightened predisposition to developing Alzheimer’s. A gene called apolipoprotein E, for instance, comes in three variants: one kind seems to reduce the risk of Alzheimer’s while another increases it. Other genes – variously associated with the body’s uptake of cholesterol, its propensity to engender inflammation and the efficiency of communication between neurons – also have a role to play in raising or lowering the chances of onset.

However, the interplay between genetic factors, environmental factors and what appears to be pure luck makes foreknowledge of whether Alzheimer’s will strike any individual impossible. It’s no wonder that the US National Institutes of Health does not generally recommend genetic testing as a worthwhile route for anyone wanting to know their future. After all, a result that indicates you are more likely than the average person to develop dementia is, in many ways, little more than a heavy psychological burden, to be borne until the symptoms start to appear – a scenario that keeps you stressed (a grave health risk) even if onset never happens. If the drugs don’t work yet, why would anyone sign up to be tested?

In the absence of a reliable test or cure, the best advice seems to be to delay ageing as much as possible, particularly where cardiovascular health is concerned. It’s an observation that fits with last month’s breakthrough. The plaque-provoking pathogens reach the brain through the weakening of the blood-brain barrier, a wall of cells that wraps around blood vessels and prevents foreign bodies from passing into the brain’s circulatory system. This weakening happens with age, suggesting that action to delay the degradation of the cardiovascular system will also delay the onset of Alzheimer’s disease.

Here, at least, we have some good news: the rate of appearance of dementia cases seems to be in decline. This may be a spin-off of our attempts to cut deaths from heart disease. It seems that as we take control of blood pressure and cholesterol levels, making significant improvements to our heart and circulatory function, we are unwittingly improving our cerebral health, too – almost certainly because the brain requires good blood flow to operate well.

The surest way to avoid Alzheimer’s, then, is simple to state and impossible to achieve. All you have to do is stay young. 

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

This article first appeared in the 23 June 2016 issue of the New Statesman, Divided Britain