Researchers from the University of Turku and Åbo Akademi University in Finland and the University of Wisconsin in the United States demonstrated that individuals who had childhood epilepsy have an increased accumulation of brain amyloid later in life, potentially predisposing them to late-onset brain amyloid disorders, such as Alzheimer's disease.

The accumulation of beta-amyloid protein in the brain is considered an early pathological brain change in Alzheimer's disease, although the exact cause of amyloid accumulation is unknown.

The study from the University of Turku, Åbo Akademi University, and University of Wisconsin is based on a globally unique population-based cohort, collected by young child neurologist, now Professor Emeritus Matti Sillanpää, who still leads the cohort. The cohort has monitored the health and social prognosis of individuals who had childhood epilepsy since the early 1960s and their matched controls since 1992. The follow-up is conducted progressively at regular intervals in collaboration with domestic and international researchers (TACOE project).

The recent collaborative study examined the brain amyloid accumulation of these individuals, who were on the verge of retirement or already retired, and their controls.

In the previous timepoint of the study (2013–2016), after 50 years of follow-up, researchers observed that individuals with childhood epilepsy had more amyloid plaques in their brains than the controls.

“The finding was the first of its kind globally, and it was unclear at that point whether the abnormal amyloid accumulation in the brain would continue, further predisposing these individuals to the development of memory disorders. This motivated our current study,” explains one of the key figures in the study, Professor of Neurology Juho Joutsa from the University of Turku.

Increased probability of abnormal amyloid accumulation in individuals with childhood epilepsy

The recent study was conducted approximately seven years after the previous timepoint, with the participants being 60–65 years old. The study included 82 percent of the previous participants, a total of 36 individuals with childhood-onset epilepsy, and 35 controls.

In the patient group, abnormal amyloid accumulation was observed in nearly one-third of the participants, whereas only 11 percent of the controls showed this accumulation. During the seven-year follow-up, the patient group accumulated more amyloid in the brain than the controls. The patient group also performed worse in cognitive tests compared to the controls, but this was not linked to the amount of amyloid plaques.

“This suggests that the amyloid accumulation in the brain has not yet led to memory disorders,” explains Joutsa.

Unique cohort study enables long-term monitoring of changes

The unique cohort utilised in the study has provided extensive information about childhood epilepsy and its prognosis over decades.

Modern brain imaging methods, which now enabled the study of brain amyloid pathology, were developed decades after the cohort was established. A recently graduated physician, now Professor of Neurology Juho Joutsa, was recruited for brain imaging analyses in the early 2010s.

The study results provide unique new information about the very long-term effects of childhood epilepsy on the brain, and the follow-up continues.

“This study is also an excellent example of what can be achieved scientifically through long-term commitment of both participants and researchers, as well as collaboration across disciplines and generations of researchers,” says Joutsa.