What capuchin monkey brains reveal about Alzheimer’s – 04/11/2024 – Balance and Health
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A group of Brazilian scientists has just discovered that yellow capuchin monkeys (Sapajus libidinosus), a species typical of Brazil and Bolivia, also develop Alzheimer’s disease.
The researchers analyzed the brains of three primates of this species who died at 9, 29 and 33 years old, respectively.
In the two older individuals, the tests detected the presence of two typical markers of this dementia: the accumulation of beta-amyloid proteins and TAU.
In Alzheimer’s, beta-amyloid accumulates in the space between neurons, while TAU occupies the interior of nerve cells — which eventually leads to their death.
The loss of these cells that make up the brain leads to the progression of typical symptoms of the disease, such as forgetfulness and difficulties in reasoning.
The discovery about yellow capuchin monkeys could open up new research perspectives for the development of diagnostic tests and medicines against Alzheimer’s, experts believe.
Neurologist Roberta Diehl Rodriguez, who is the first author of the research, published on March 15 in the specialized journal Scientific Reports, from the Nature group, explains that the project began as a result of an alliance between the two Brazilian universities.
On the one hand, UnB (University of Brasília) has a Primatology Center, which specializes in evaluating different types of monkeys.
On the other, USP (University of São Paulo) houses an important Neurology Department, with advanced equipment to carry out different types of scientific investigations.
“The UnB Primatology Center carries out a series of psychological and functional tests with the monkeys. However, when the animals died, they had never been able to examine their brains”, she says.
“During a conference, professor Ricardo Nitrini [da USP] spoke with professor Maria Clotilde Tavares [da UnB]and they had the idea of forming this partnership, which started in 2018”, explains the doctor.
Rodriguez highlights that, when analyzing what had previously been published about capuchin monkeys, there was not much information about their brains and their risk of developing dementia.
“And it’s one of the most intelligent New World monkey species we know of,” she notes.
The New World monkeys are a group that designates the species of primates typical of the American continent.
Some studies published in recent decades show the advanced cognitive capacity of this primate, which lives mainly in the Northeast and Central-West regions of Brazil.
They are capable, for example, of producing stone tools, used to crack nuts and other hard foods, as well as splitting trunks and branches to facilitate access for insects and larvae.
Yellow capuchin monkeys can also stay in a bipedal position for a long time and use sticks to get food, honey and water.
In mangrove regions, they use pieces of wood to break open shells and mollusks.
“Wild or captive capuchin monkeys were subjected to various cognitive tests, which revealed strengths in working memory, learning, recall, executive function and problem solving,” the newly published study lists.
“They demonstrate the ability to learn independently, through exploratory tendencies, as well as the ability to learn by observing older individuals. Furthermore, they may present behavioral modifications due to cohabitation with humans”, adds the text.
Invaded brain collapsing
As mentioned at the beginning of the report, scientists carried out analyzes and tests with the brains extracted from three yellow capuchin monkeys that died from other causes at 9, 29 and 33 years of age.
And the work revealed that these animals may present a condition similar to what is observed in the heads of human beings affected by Alzheimer’s.
The 9-year-old monkey, the youngest in the group, had no changes, while the oldest monkeys, aged 29 and 33, showed the typical changes of the disease, such as inflammation and the accumulation of harmful proteins.
In the wild, a capuchin monkey has a life expectancy of 34 to 36 years. Once in captivity, he can live until 55.
In summary, this type of dementia is marked by two main stages. First, beta-amyloid protein accumulates on the outside of neurons. Second, the TAU protein starts to be stored inside these cells.
This entire process is harmful and causes the death of these brain units. Little by little, as this condition evolves, the individual begins to lose their memories and the ability to reason.
To date, available medications only act on some specific symptoms of dementia and are not capable of stopping the progression of symptoms.
There is only one drug recently approved in the USA that has been shown to be capable of “clearing” beta-amyloid from the brain, with a possible cognitive improvement in the patient — but it is expensive and is restricted to early, almost asymptomatic cases, whose diagnosis is very difficult. difficult.
Called lecanemab (from Eisai and Biogen laboratories), this medication is not yet released in Brazil.
For a long time, scientists believed that Alzheimer’s, with the entire package of brain deterioration involved, was a disease exclusive to humans.
But recently, studies were published that debunked this idea. Nowadays, it is known that chimpanzees also develop the condition, as do yellow capuchin monkeys, as revealed in the USP and UnB study.
Aggregates of TAU protein have also been observed in mouse lemurs (Microcebusa type of primate from Madagascar) and neurofibrillary tangles typical of this dementia in rhesus monkeys (mulatta macaque) and vervet (Chlorocebus pygerythrus).
New possibilities and next steps
The experts interviewed by BBC News Brasil highlight that, until now, basic research into Alzheimer’s was carried out with mice or rats.
But there’s a problem here: these rodents don’t naturally develop this type of dementia.
Scientists then needed to cause genetic mutations so that these guinea pigs would have one or more of those markers of the disease, such as the accumulation of beta-amyloid.
“However, even when modified, mice and rats do not develop Alzheimer’s themselves and all those changes that we commonly see in the human brain”, says neurologist Sonia Brucki, another author of the study.
In other words: even though they are the best option available to date, these animals were far from the ideal scenario when we think about studies to understand Alzheimer’s, or eventually discover better ways to prevent, diagnose and treat the condition.
“Having animals that develop the pathology like humans would allow testing of new treatments, in addition to possible advances in the knowledge of biomarkers of the disease’s evolution”, predicts the doctor.
And that’s where yellow capuchin monkeys come in: studying this species’ brain in depth could help understand how Alzheimer’s develops. Furthermore, these primates can serve as guinea pigs in studies of potential new medicines.
“The advantage of capuchin monkeys is that they are much smaller than chimpanzees, and their maintenance in captivity is much simpler and cheaper,” explains Brucki.
“Plus, they are not at risk of extinction,” she adds.
The work of USP and UnB is just in its first steps. The analysis of the brains of these three primates served to confirm the hypothesis that they develop Alzheimer’s and to standardize values and parameters for future investigations.
From now on, the team of scientists wants to thoroughly investigate other individuals of the same species that eventually die over the months and years – they will not euthanize these animals.
Another ambition of the group is to evaluate the brains of monkeys while they are still alive using imaging tests, such as magnetic resonance imaging.
The objective here is to carry out periodic monitoring to understand when signs of Alzheimer’s begin to appear in the brain — and how this translates into practice, through symptoms, such as low activity or difficulties using tools as they get older.
“We want to know how the pathological processes that occur in Alzheimer’s disease in other species can establish concepts of aging”, concludes Brucki.
The text was originally published here.
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