Dr. Aniko Korosi

Dr. Aniko Korosi is a distinguished neuroscientist and associate professor at the University of Amsterdam whose innovative work bridges developmental neurobiology, stress biology, nutrition, and cognitive health. Her research focuses on how early-life stress affects brain development and lifelong cognitive function, with particular emphasis on the role of metabolic signals, nutrients, and immune-related mechanisms in modulating vulnerability to disorders such as Alzheimer’s disease and depression. Dr. Korosi leads an interdisciplinary team that combines preclinical models and human studies to uncover biological pathways and explore nutritional or peripheral interventions that might prevent or reverse the lasting impacts of early adversity. It is an honor to share her expertise with the ELePHiNt community in this interview — enjoy!

Q1: Why is it important to study early life stress? 

A1: “Early life adversity is one of the key risk factors for the development of several different psychiatric disorders”, says Dr. Korosi, “and it’s also a risk factor for other metabolic health problems like obesity and other diseases.” She also mentions Alzheimer’s disease as an early-life-stress-associated illness, which is central to her work. 

Dr. Korosi goes on to note that early life adversity shapes not only disease risk, but also disease biology—advocating for more informed interventions. “There is also the idea that early life adversity might [trigger] these disease states and that [the disease may present with] a somewhat different biological profile [...] At the moment, while we can maybe identify the individuals at risk, we don’t have any targeted interventions for the individuals who develop these diseases partly because of their [exposure to] early life adversity. It’s not quite personalized intervention, but I think stratification of the interventions might be necessary to make them more effective.” 

Q2: How did early life adversity become linked to aging and Alzheimer’s disease in your work?

A2: Dr. Korosi states that her work stemmed from the longstanding debate that early life adversity potentially triggers accelerated aging, with early evidence pointing to cognitive decline and aged biological phenotypes following adverse experiences early in life. “I got intrigued by this idea that something that we normally really conceptualize as a disease of [old age] also might have origins in early life adversity exposures. So we started to test it first in a really classical Alzheimer’s mouse model.” Dr. Korosi describes the findings of this work, which demonstrate that exposure to early life adversity could worsen amyloid pathology, even in transgenic mice predisposed to overexpress amyloid proteins. She situates these findings within a growing interest in neuroinflammation and microglia. “We had already started to focus a lot on neuroinflammation or microglia, knowing that neuroinflammation plays a really important role in a broad spectrum of diseases […] including Alzheimer’s disease. And already by then, we were playing with the idea that early life adversity might prime microglia similarly to an early life infection.” All the same, Dr. Korosi is quick to note that early life stress is not purely pathological. “I rather refer to the consequences of early-life adversity as adaptive changes…changes [to] some developmental trajectories which might also have an adaptive value and beneficial consequences for the individual. [...] When it becomes maladaptive depends on a lot of additional aspects—genetic makeup [for example] and all the exposome from the rest of life.”

Q3: Do microglia retain a ‘memory’ of early life adversity? 

A3: “I would have envisioned that maybe some of these effects stem from microglia, and that would then be broken down to other effects” says Dr. Korosi, “but based on the studies that we did, it would seem that it [doesn’t work] that way. [...] At postnatal day nine, immediately after early life adversity, we saw relatively minimal changes in microglia, and we saw a lot more changes later in life, suggesting that other trajectories or other changes are occurring at the level of synapses and other processes, and that that might change the microenvironment, [which] might then trigger microglial changes and altered response later on.” Dr. Korosi notes that these findings may be limited by certain technical challenges inherent to studying microglia. “[Microglia are] these fantastic cells that are able to integrate so much different information from their microenvironment [...] but then studying them while being removed from this microenvironment might greatly impact the outcomes. As for which of the specific signals from the early-life adversity might then prime microglia; that is a challenge by itself, as this is already so complex.” In her opinion, the precise factors linking microglial changes to the lasting impact of early life stress remain to be seen. Her more recent work, however, suggests that age might play a critical role. “The strongest determinant of differential gene expression in microglia was age” says Dr. Korosi, “[...] more than stress or an immune challenge in the form of LPS, for example.”

Q4: How could your work in nutrition be implemented as an intervention following early life adversity? 

A4: According to Dr. Korosi, nutritional interventions offer a potentially complementary strategy that operates through fundamentally different principles than classical pharmacology. “This part of the research really came from my inspiration [by] nutritional psychiatry,” she begins, referring to the growing body of literature investigating the role of nutrient intake in mental health outcome and modulation. “What I realize more and more when you read nutritional intervention studies [however] is that it works fantastically for some, but not for others, and we have no idea why that is.” Another significant hurdle in the implementation of this strategy, says Dr. Korosi, is the general air of skepticism surrounding nutrition-based intervention, stemming largely from the lack of clearly defined mechanisms of action. “If you think about any other intervention strategies, they are usually really targeted, right? Like, for a specific receptor, [you’d have] an agonist and antagonist, all these pharmaceutical compounds [which] are very targeted, therefore it's easier to [gain a] mechanistic understanding of how [the intervention] works. And I think with nutrients, there is a lot of skepticism, even from experts, because, due to their broader actions, it’s harder to really pinpoint the one specific mechanism driving their effects as clearly”. 

Dr. Korosi's work aims to fill these gaps in knowledge, targeting nutrients one by one to gain a more specific mechanistic understanding of their impact on the brain, specifically in the context of early life and early life stress. “What surprised me the most is that even when you take one nutrient at a time, they can be [exceptionally] powerful; they can have a beneficial effect even when you make one subtle change. We are not doing anything supraphysiological—that’s the power of this strategy. It really exploits the [inherent] biochemical properties of these nutrients, which can act on a broad range. It’s not one receptor on one cell type. And it’s use or lose — if it’s needed, it’s being used.” 

In time, Dr. Korosi hopes to see this type of intervention being implemented in concert with current first-line treatments, such as pharmacology or life-style changes. “I think now everybody [is starting to realize] that fifty to seventy years of neuropharmacology didn't deliver as much as we hoped, so we need additional [strategies] [...] and lifestyle is great, but lifestyle changes are often hard to achieve, and not always possible for a variety of reasons. So it's nice to have additional tools.”

Q5: Were there any findings in your work that fundamentally changed how you think?

A5: For Dr. Korosi, the most striking shift came from seeing how subtle early life interventions could rival the impact of major life experiences. “At the very beginning, when I started the nutrition related projects, I was skeptical myself. It made sense to me [conceptually], but to see how consistently big the effect is of just a really subtle change early in life — months before — and that this is able to modulate behavior and protect against the impact of early life adversity–induced cognitive decline, remains very striking to me.” Like many, Dr. Korosi initially suspected that small changes in any one specific nutrient group would be too subtle to influence something as significant as exposure to adversity. “The fact that this can have such a powerful effect has really changed the way I think about [this field] and how to exploit [it].”

Q6: What current projects and directions are you most excited about now?

A6: Dr. Korosi’s future work aims to merge these projects, and move towards potential prevention strategies. “Having seen all the positive effects of the early diet in the context of early life adversity made us think: can we also make the system more resilient? Can we interfere with the progression of Alzheimer’s pathology in our mouse model? [...] If you acknowledge that early life is a really sensitive period also for such a disease, then that opens a lot of opportunities.” Of course, as Dr, Korosi notes, this approach is not without its challenges. “Early life has its beauty in its difficulty. Lifetime interventions are very difficult to translate, [but] early life is a period where implementation might actually be realistic. [Prior to onset], there are a lot of opportunities for prevention. And not only to protect the vulnerable ones, but to build resilience in general.”

Interview conducted by: Elisa Gonçalves de Andrade

Blog post written and edited by: Dominique Lumley