A review in the NYTimes:

A Descent Chronicled With Care

‘First Cousin Once Removed’ Documents Edwin Honig’s Life

Directed by Alan Berliner – 1 hour 18 minutes; not rated

“Recalling who I was, I see somebody else” begins a poem by Fernando Pessoa, quoted in Alan Berliner’s “First Cousin Once Removed.” In Mr. Berliner’s moving and mysterious documentary, the poet and translator Edwin Honig picks his way through his mind and memories in the falling shadow of Alzheimer’s. It’s the latest of Mr. Berliner’s dogged investigations into identity and family, and his strongest work yet, elevated by the presence of another artist in Mr. Honig, playfully insightful and eloquent even as his powers wane.

Mr. Honig, who was 91 when he died in 2011, is interviewed in the peaceful solitude of humble living quarters, by a window with a view of rustling trees. A nimble montage of Mr. Berliner’s visits — Mr. Honig was his cousin — neatly establishes an award-winning poet’s failing memory and yet open mind, as well as a filmmaker’s touching persistence.

“Mirror, mirror, on the wall,” Mr. Berliner says at one point in the stop-and-start questions and answers that follow. “You be camera, and I’ll be all,” Mr. Honig responds.

Mr. Honig cuts a striking figure in the film, with his aquiline nose, shock of white hair and knowing gaze, making it easy to picture him in the past as a professor, critic and mentor. Into the oblivion of advanced age, he freestyles poetry and offers frank answers or blank verbal shrugs. But Mr. Berliner, like a painter working at different times of day, also shows Mr. Honig speechless, making birdlike noises or simply drumming on the arms of his chair.

Careful montage shapes these views of Mr. Honig and interviews with family members and friends into a sensitive, unified portrait of a poet and a human being. Language and self come across as intertwined and (as for all of us) perhaps more unstable or fluid than we like to admit. Yet even when all else has failed, rhythm and sound endure for Mr. Honig (the drumming, the noises). Mr. Berliner’s use of typewriter key-punches and pings — a sonic motif he has used before — never lets text and writing fade from the story.

Mr. Berliner doesn’t shy from specifics of his cousin’s life — from Mr. Honig’s hardheaded cantor father to the two children he adopted with his second wife, only to be mercilessly critical as they grew. And since Mr. Honig’s family members are, in a roundabout way, Mr. Berliner’s, the movie enters into a generational dialogue with this filmmaker’s ongoing project in cinematic genealogy. “First Cousin Once Removed” echoes “Nobody’s Business,” Mr. Berliner’s 1996 movie about his hilariously resistant father (who appears briefly here, considerably subdued), or “Intimate Stranger,” his 1991 attempt to reconstruct his Sephardic maternal grandfather’s history.

Mr. Berliner’s son Eli also appears, playing with a delighted Mr. Honig, and one can sense a certain urgency in the filmmaker’s compassion — a desire to draw out his cousin that approaches need. It’s an urge to communicate, even commune, that one can readily sympathize with, and Mr. Berliner’s film bravely brings us to the edge of language and experience.

ANOTHER RECENT FILM, THE GENIUS OF MARIAN by Banker White (will play at the St. Louis International Film Festival) – the trailer:

AND THE 1994 CLASSIC, “COMPLAINTS OF A DUTIFUL DAUGHTER“

MORE NEWS ABOUT ALZHEIMER’S

The discovery of the first chemical to prevent the death of brain tissue in a neurodegenerative disease has been hailed as the “turning point” in the fight against Alzheimer’s disease.

More work is needed to develop a drug that could be taken by patients.

But scientists say a resulting medicine could treat Alzheimer’s, Parkinson’s, Huntington’s and other diseases.

In tests on mice, the Medical Research Council showed all brain cell death from prion disease could be prevented.

Prof Roger Morris, from King’s College London, said: “This finding, I suspect, will be judged by history as a turning point in the search for medicines to control and prevent Alzheimer’s disease.”

He told the BBC a cure for Alzheimer’s was not imminent but: “I’m very excited, it’s the first proof in any living animal that you can delay neurodegeneration.

“The world won’t change tomorrow, but this is a landmark study.”

Cells starveThe research team at the Medical Research Council Toxicology Unit, based at the University of Leicester, focused on the natural defence mechanisms built into brain cells.

When a virus hijacks a brain cell it leads to a build-up of viral proteins. Cells respond by shutting down nearly all protein production in order to halt the virus’s spread.

However, many neurodegenerative diseases involve the production of faulty or “misfolded” proteins. These activate the same defences, but with more severe consequences.

The misfolded proteins linger and the brain cells shut down protein production for so long that they eventually starve themselves to death.

This process, repeated in neurons throughout the brain, can destroy movement or memory or even kill, depending on the disease.

This process is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases.

The researchers used a compound which prevented those defence mechanisms kicking in and in turn halted neurodegeneration.

Analysis

It is rare to get cautious scientists keen to describe a study in mice as a turning point in treating Alzheimer’s.

It is early science, a lot can go wrong between a drug for mice and a drug for humans and the only published data is for prion disease, not even Alzheimer’s.

So why the excitement?

It is the first time that any form of neurodegeneration has been completely halted, so it is a significant landmark. It shows that the process being targeted has serious potential.

If this can be successfully developed, which is not guaranteed, the prize would be huge.

In Parkinson’s the alpha-synuclein protein goes wrong, in Alzheimer’s it’s amyloid and tau, in Huntington’s it’s the Huntingtin protein.

But the errant protein is irrelevant here as the researchers are targeting the way a cell deals with any misfolded protein.

It means one drug could cure many diseases and that really would be something to get excited about.

The study, published in Science Translational Medicine, showed mice with prion 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.

Lead researcher Prof Giovanna Mallucci told the BBC news website: “They were absolutely fine, it was extraordinary.

“What’s really exciting is a compound has completely prevented neurodegeneration and that’s a first.

“This isn’t the compound you would use in people, but it means we can do it and it’s a start.”

She said the compound offered a “new pathway that may well give protective drugs” and the next step was for drug companies to develop a medicine for use in humans.

‘Very dramatic’Prof Mallucci’s lab is also testing the compound on other forms of neurodegeneration in mice but the results have not yet been published.

Side effects are an issue. The compound also acted on the pancreas, meaning the mice developed a mild form of diabetes and lost weight.

Any human drug would need to act only on the brain. However, this gives scientists and drug companies a starting point.

David Allsop, professor of neuroscience at Lancaster University described the results as “very dramatic and highly encouraging” but cautioned that more research was needed to see how the findings would apply to diseases such as Alzheimer’s and Parkinson’s.

Dr Eric Karran, the director of research at the charity Alzheimer’s Research UK, said: “Targeting a mechanism relevant to a number of neurodegenerative diseases could yield a single drug with wide-reaching benefits, but this compound is still at an early stage.

“It will be important for these findings to be repeated and tested in models of other neurodegenerative diseases, including Alzheimer’s disease.”

Pioneering brain imaging that can detect the build-up of destructive proteins linked to Alzheimer’s has been developed by Japanese

It could lead to new ways of diagnosing the condition and of testing the effectiveness of new drugs.

The technology, reported in the journal Neuron, can identify inside a living brain clumps of a protein called tau that is closely linked to the disease.

Alzheimer’s Research UK said it was promising work.

Alzheimer’s disease is a problem for researchers trying to come up with a cure. The brain starts to die years before any symptoms are detected, which means drugs are probably given too late.

A diagnosis of Alzheimer’s cannot be made with absolute certainty until a patient has died and their brain is examined. It is also not 100% clear what is the cause of the dementia and what are just symptoms.

One protein, called tau, is very closely linked to the disease, with tangles of tau thought to be one way in which brain cells are killed.

The team, lead by the National Institute of Radiological Sciences in Chiba, used positron emission tomography to build a 3D picture of tau in the brain.

They developed a chemical that could bind to tau and then be detected during a brain scan.

Finding tau in the brain

Tests on mice and people with suspected Alzheimer’s showed the technology could detect tau.

Dr Makoto Higuchi, from the National Institute of Radiological Sciences in Japan, said: “Positron emission tomography images of tau accumulation… provide robust information on brain regions developing or at risk for tau-induced neuronal death.”

The research is at an early stage, but it could eventually lead to an actual test for Alzheimer’s disease.

It might also allow researchers to closely follow the impact drugs that affect tau have on the brain.

Another protein – beta amyloid – is also linked to Alzheimer’s and can be detected in similar tests.

Dr Eric Karran, director of research at Alzheimer’s Research UK, said: “This promising early study highlights a potential new method for detecting tau – a key player in both Alzheimer’s and frontotemporal dementia – in the living brain.

“With new drugs in development designed to target tau, scans capable of visualising the protein inside the brain could be important for assessing whether treatments in clinical trials are hitting their target.

“If this method is shown to be effective, such a scan could also be a useful aid for providing people with an accurate diagnosis, as well as for monitoring disease progression.”