Imagine you cooking one noodles at home: if it is not cooked under ideal conditions, there is the possibility of it sticking together, forming a mass that is difficult to eat. Something similar happens with Alzheimer’s disease.
We know, for example, that the brains of Alzheimer’s patients accumulate two proteins that characterize the disease: b-amyloid (present in lesions known as amyloid plaques) and tau (components of neurofibrillary tangles).
Although we all have these proteins in our brains from birth, they acquire abnormal shapes in the brains of patients.
In the case of patients, b-amyloid and tau in the brain form clumps that no longer function correctly and also contribute to brain cells, including neurons, malfunctioning.
This leads to difficulty in communication between neurons through synapses. Such changes begin to happen years or decades before the initial symptoms appear.
The discovery
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The first report of Alzheimer’s disease was made in 1906 by the German psychiatrist after whom the disease is named: Alois Alzheimer. In addition to being a doctor, he was a scientist who had received training with important scientists of the time in Germany: Franz Nissl and Emil Kraepelin.
When the Alzheimer’s doctor was working at the Frankfurt asylum, he received the case of patient Auguste Deter, a woman in her 50s presenting with mental confusion, changes in behavior, as well as progressive memory loss. The patient died in 1906 and Alois Alzheimer had access to her brain.
With the scientific knowledge he had, Alois Alzheimer made associations that are still considered fundamental characteristics of Alzheimer’s disease today.
He observed that regions of Auguste’s brain were atrophied, with fewer neurons than expected, in addition to describing two types of lesions known as senile plaques (or amyloid plaques) and neurofibrillary tangles.
The presentation of this curious case at a psychiatry conference in Germany was marked as the first record of the disease.
Today, it is known that Alzheimer’s patients have progressive cognitive impairment that evolves to affect other brain functions such as mood, executive capacity, among others, until it causes loss of autonomy and, eventually, leads to death.
The era of anti-amyloid therapies
Although we still don’t have a cure more than a hundred years since Alzheimer’s was originally described, science has advanced considerably. Since the 1980s, science has invested a lot of effort in understanding Alzheimer’s.
Today we better understand the risk factors, the brain changes that occur in the disease and how to better identify it.
It is natural to imagine, therefore, that a lot of effort in science and medicine has focused on finding therapies that eliminate b-amyloid and tau clumps.
In the early 2000s, influential work in the field demonstrated that the use of monoclonal antibodies to sequester b-amyloid and target it for elimination had a therapeutic effect on laboratory animals with Alzheimer’s symptoms. This was the beginning of what we call anti-amyloid immunotherapies.
After much more research and the involvement of pharmaceutical companies, a new Alzheimer’s drug — the first since 2003 — was controversially approved by the US Food and Drug Administration (FDA) for use in humans in 2021.
It was called Aducanumab and, although efficient in reducing amyloid plaques in patients, its clinical use showed that it was still not as efficient in alleviating the symptoms of the disease.
What seemed like a bucket of cold water, however, was the beginning of a new generation of anti-amyloid drugs with increasingly greater effectiveness.
A few years later, two new drugs (Donanemab and Lecanemab) also proved to be effective in reducing amyloid plaques and other markers of Alzheimer’s, as well as being the first to act on the causes of the disease and reduce its progression.
It is true that the effects are still modest. Average 30-35% reduction in progression over an 18-month interval in early stages of the disease. And the cure does not yet exist, but such advances are encouraging.
Both drugs were approved by the FDA and, in 2025, by Anvisa in Brazil.
One caveat must be made: these medications still have a very high cost and are not recommended for all patients. Doctors need to make a very careful analysis to prescribe this treatment.
Brazilian science in the study of Alzheimer’s
In addition to new and more effective treatments, we need to investigate more accurate diagnostic approaches, more applicable prevention strategies and also better understand how the disease sets in and evolves.
In this aspect, something we should celebrate is the prominence that Brazilian laboratories have had over the last decade among the scientific community in Alzheimer’s disease and related dementias.
Our group at UFRJ demonstrated, for example, a then unknown mechanism through which physical exercise protects the brain against neurodegenerative processes in Alzheimer’s.
Irisin is a hormone produced by both muscles and the brain during physical exercise.
It acts on our brain cells and strengthens communication between neurons. This is important because a sedentary lifestyle is one of several modifiable risk factors to reduce the chance of developing Alzheimer’s.
Why does understanding Alzheimer’s in Brazil require Brazilian data?
Much of the information we have about Alzheimer’s was generated abroad, notably in research centers such as the United States, Sweden and the United Kingdom.
Therefore, it is possible to imagine that not everything discovered in these countries directly applies to the Brazilian population, which is culturally and genetically diverse. Thus, much of the most recent effort by Brazilian researchers has been dedicated to getting to know our population.
This approach is already bearing fruit: today we know the main modifiable risk factors in Brazil and we are already validating blood biomarkers in Brazilians.
Furthermore, a law establishing a national care and research plan for dementia was sanctioned by the federal government in 2024 and the scientific and medical community has discussed with interest the ways of implementing this policy.
This is a time of great hope and action to improve the treatment and care of patients with dementia and we should be proud that Brazilian scientists are contributing to the forefront of knowledge in the area.
This text was published in The Conversation. Click here to read the original version
date:2026-02-12 01:00:00
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