Amyloid-β: a potential link between epilepsy and cognitive decline.

Area of Science:

• Neuroscience
• Neurology
• Pathology

Background:

• Late-onset epilepsy is associated with an increased risk of dementia.
• Seizures are observed in early stages of Alzheimer disease (AD), suggesting an epileptic AD prodrome.
• The relationship between epilepsy and cognitive decline is debated, with uncertainty regarding causality and shared underlying mechanisms.

Purpose of the Study:

• To review evidence linking amyloid-beta (Aβ) to a shared pathway between epilepsy and cognitive decline, particularly in AD.
• To explore the hypothesis that Aβ mediates a continuum from epilepsy to cognitive decline.
• To discuss the potential of Aβ assessment and cognitive testing for risk stratification in late-onset epilepsy.

Main Methods:

• Literature review of studies on epilepsy, cognitive decline, and amyloid-beta (Aβ) pathology.
• Examination of experimental evidence for Aβ-mediated epileptogenic alterations.
• Discussion of clinical observations and hypotheses regarding the Aβ-epilepsy-dementia continuum.

Main Results:

• Individuals with epilepsy exhibit increased brain Aβ pathology.
• Aβ-mediated alterations can promote epileptogenesis, potentially starting at the soluble stage before plaque formation.
• Aβ is proposed as a key factor in the continuum of epilepsy and cognitive decline.

Conclusions:

• Amyloid-beta (Aβ) may represent a shared pathway linking epilepsy and cognitive decline, especially in Alzheimer disease (AD).
• Early assessment of Aβ levels and cognitive function in late-onset epilepsy could aid dementia risk stratification.
• Late-onset epilepsy patients may be a suitable cohort for testing preventive strategies against cognitive decline.