Eye-tracking-based cognitive assessment efficiently detects mild cognitive decline in the predementia stage.

INTRODUCTION: The early detection of cognitive decline is key to maximizing the benefits of preventive and therapeutic interventions against dementia. Generally, dementia is first assessed by interview-based neuropsychological tests, but the lengthy interview and mental stress during the assessment process make screenings inefficient. We previously developed a rapid screening test for dementia using an eye-tracking technology (eye tracking-based cognitive assessment, ETCA) and reported its utility for clinically detecting cognitive impairment in dementia cases. However, the ETCA's performance in detecting people with mild cognitive decline, which is the major target population for dementia-prevention strategies, remains insufficiently examined. Therefore, this study aimed to evaluate the ETCA's performance in individuals aged 40 years and older (n = 94, mean age; 61.0 [SD 13.1] years) without being formally diagnosed with dementia. METHODS: All participants underwent both the ETCA and neuropsychological tests, including the Mini-Mental State Examination (MMSE), Rivermead Behavioral Memory Test (RBMT), and Addenbrooke's Cognitive Examination-III (ACE-III) on the same day. We examined the correlations in scores between the ETCA and each neuropsychological test. Furthermore, we selected participants who earned normal scores in each neuropsychological test and evaluated the ETCA's performance in this subgroup. RESULTS: Participants' ETCA scores correlated significantly with their scores on neuropsychological tests, including the MMSE, RBMT, and ACE-III. Notably, the ETCA scores correlated with the RBMT or ACE-III scores in individuals who showed normal scores in each neuropsychological test. CONCLUSION: The ETCA has the potential to screen mild cognitive decline efficiently at the predementia stage in nonclinical settings.

Antiepileptic Drugs Modulate Alzheimer-Related Tau Aggregation in a Neuronal Activity-Independent Manner.

INTRODUCTION: A rapidly increasing number of patients with dementia present a serious social problem. Recently, the incidence of epilepsy in patients with Alzheimer's disease (AD) is increasing, drawing attention to the pathological relationship between the two conditions. Clinical studies have suggested the protective action of antiepileptic agents on dementia; however, the underlying mechanism remains unknown. We evaluated the effects of multiple antiepileptic drugs using tau aggregation assay systems to determine the effects of antiepileptic agents on tau aggregation, a major neuropathological finding associated with AD. METHODS: We evaluated the effects of seven antiepileptic agents on intracellular tau aggregation using a tau-biosensor cell-based high-throughput assay. Next, we tested these agents in a cell-free tau aggregation assay using thioflavin T (ThT). RESULTS: The assay results revealed that phenobarbital inhibited tau aggregation, whereas sodium valproate, gabapentin, and piracetam promoted tau aggregation. In the cell-free tau aggregation assay using ThT, we confirmed that phenobarbital significantly inhibited tau aggregation. CONCLUSION: Antiepileptic drugs may modify the tau pathology in AD in a neural activity-independent manner. Our finding may provide an important insight into the optimization of antiepileptic drug therapy in older adults with dementia.