Alzheimer's: The Hell That Resists a Cure

Alzheimer's: The Hell That Resists a Cure

In 1906, German neuropsychiatrist Alois Alzheimer peine the skull of a patient who had died of an "unusual mental illness." What he saw under the microscope – protein tangles and sticky plaques – gave a name to the pathology that today strips the memory of 55 million people worldwide. More than a century later, Alzheimer's remains a hell from which there is no escape: there is no cure, diagnosis comes too late, and the real causes remain a minefield between official science and heterodox hypotheses.

The Causes: Aluminum, Fungi, or a Clogged Cleaning System

From the earliest days of the thread, the question of origin divides opinion. One current points to aluminum: autopsies of patients have found the metal in the brain, and it is speculated that it arrives via intramuscular injections. Another hypothesis suggests fungal infections – Candida albicans – or viral ones – herpes simplex – as triggers. The idea is that amyloid plaques would not be the cause, but rather the defensive response of neurons to an as-yet-unknown attacker. "Amyloid plaques form as a defense of neurons against the attack of that killer vector," summarizes one analysis of the debate. The glymphatic system – the brain's "cleaning crew" – has also entered the scene: if it fails, protein waste accumulates and triggers the neurodegenerative cascade. Meanwhile, the dominant theory – beta-amyloid accumulation – is piling up criticism: there are people with plaques but no Alzheimer's, and patients with Alzheimer's but no plaques.

Diagnosis: Blood Speaks Before Symptoms

The only good news recently comes from early diagnosis. The U.S. FDA approved Roche's Elecsys pTau181 test, which measures a phosphorylated form of the tau protein in blood. A simple blood test can detect brain damage before the first forgetfulness appears. "Brain damage caused by Alzheimer's can be detected before the first clinical symptoms appear through a blood test," according to a study published in Nature Medicine. The test, available since 2026, eliminates the need for lumbar punctures and opens the door to mass screening. The problem: without an effective treatment, knowing earlier only serves to prolong the anguish.

Treatments: Donanemab, Methylene Blue, and the Promise of NAD+

On the therapeutic front, caution reigns. Donanemab, a monoclonal antibody, manages to slow cognitive decline in early stages, but it is not a cure. "The pharmaceutical company will make a fortune and patients won't notice a thing," says a skeptical voice. More promising seems methylene blue, a dye that already in the 80s showed the ability to dissolve tau protein filaments. A study with 321 patients confirmed that it prevents protein aggregation, but since it cannot be patented, its research has been left in limbo. "It is a substance that can no longer be patented and, of course, its knowledge is of no interest," they denounce. The other hopeful line is the restoration of brain NAD+, which in preclinical models reversed advanced pathology and restored cognitive function, contradicting the "deterministic view of irreversibility." Blarcamesine, also awaiting the EMA's verdict in 2026, promises to slow the disease if detected in time.

The Disconcerting Data: Declining Prevalence

And then comes the paradox. While the absolute number of cases grows due to population aging, the proportion of older adults with dementia has fallen by 30% in the last 15 years. "Before, 12 out of every 100 elderly suffered from the disease; now 8 out of every 100 do," reads an exchange. Why? No one knows for sure. Some point to reduced environmental toxins or dietary improvements; others, to the disease having been "dispersed" into more precise diagnoses. But the data is there: lower relative incidence, more mystery. Official science doesn't quite add up; heterodox hypotheses don't either. The hell remains the same, but perhaps something is changing in the trenches.