Peter Høgh

Epileptiform discharges in Alzheimer’s disease (AD) and Lewy body dementia (DLB) may be associated with cognitive decline. Iron accumulation has been implicated in neurodegenerative processes; however, its relationship to epileptiform discharges remains unknown. In addition, the relationship between iron deposition, structural brain changes, and epileptiform discharges remains unclear. The objective is to investigate whether iron deposition and structural brain atrophy are associated with epileptiform discharges in patients with AD, DLB, and healthy controls (HCs). A total of 25 patients with AD, 10 patients with DLB, and 15 HCs were included in the analysis. The participants underwent MRI including quantitative susceptibility mapping (QSM) and structural T1-weighted imaging. We examined the four regions of interest, which are tied to iron deposition and AD pathology. Ear-EEG recordings were used to quantify spike frequency (epileptiform discharges/24 h). No significant group differences were found for susceptibility across regions. Susceptibility was not associated with spike frequency. Patients with AD exhibited significant hippocampal atrophy. Higher hippocampal volume was associated with lower spike rates in adjusted models. Susceptibility and hippocampal volume were associated, and in a multilinear model with age, hippocampal volume accounted for a larger proportion of the explained variance. This study found no evidence linking iron deposition to epileptiform discharges in AD or DLB. Instead, hippocampal atrophy appears more strongly associated with epileptiform discharges, which could indicate that the underlying pathological processes rather than iron are the primary driving factor for epileptiform discharges.

Background: In patients with Alzheimer’s disease (AD) without clinical seizures, up to half have epileptiform discharges in long‐term in‐patient electroencephalography (EEG) recordings. Long‐term in‐patient monitoring is obtrusive, and expensive as compared to out‐patient monitoring. No studies have so far investigated if long‐term out‐patient EEG monitoring is able to identify epileptiform discharges in AD. To investigate if epileptiform discharges as measured with ear‐EEG are more common in patients with AD compared to healthy elderly controls (HC). To understand the association with AD, we investigated the variability across multiple recordings.Method: In this longitudinal observational study, 24 patients with mild to moderate AD and 15 age‐matched HC were included in the analysis. Patients with AD underwent up to three ear‐EEG recordings, each lasting up to two days, within 6 months. The first recording was defined as the baseline recording.Result: At baseline, epileptiform discharges were detected in 75.0% of patients with AD and in 46.7% of HC (p‐value = 0.073). The spike frequency (spikes or sharp waves/24 hours) was significantly higher in patients with AD as compared to HC with a risk ratio of 2.90 (CI: 1.77‐5.01, p<0.001). Most patients with AD (91.7%) showed epileptiform discharges when combining all ear‐EEG recordings.Conclusion: Long‐term ear‐EEG monitoring detects epileptiform discharges in most patients with AD with a three‐fold increased spike frequency compared to HC, which most likely originates from the temporal lobes. Since most patients showed epileptiform discharges with multiple recordings, elevated spike frequency should be considered a marker of hyperexcitability in AD.

Background: Mild cognitive impairment (MCI) is associated with clinical progression to Alzheimer’s disease (AD) but not all patients with MCI convert to AD. However, it is important to have methods that can differentiate between patients with MCI who

Introduction: Animal models of Alzheimer's disease show that exercise may modify β‐amyloid (Aβ) deposition. We examined the effect of a 16‐week exercise intervention on cortical Aβ in patients with mild‐to‐moderate Alzheimer's disease. Methods: Thirty‐six patients with Alzheimer's disease were randomized to either one hour of aerobic exercise three times weekly for 16 weeks or usual care. Pre and post intervention, 11Carbon‐Pittsburgh compound B positron emission tomography was carried out to assess cortical Aβ, and quantified using standardized uptake value rations (SUVRs). Results: The intervention showed no effect on follow‐up SUVRs in a covariance analysis with group allocation, baseline intervention SUVR, age, sex, and baseline Mini–Mental State Examination as predictors. Change in SUVRs did not correlate with changes in measures of physical or aerobic fitness. Discussion: The present findings do not support an effect of exercise on Aβ. However, the relatively short intervention period may account for a lack of efficacy. Further studies should test earlier and longer interventions.

This paper demonstrates how a company can implement a product platform in 35 man-days. Instead of developing a new platform, the main idea of this platform is to make decisions concerning good solutions to a product assortment, essentially by determining what is value-creating variance. The main benefits are reduced costs, reduced lead time and increased ability to focus engineering resources on aspects providing value to the customer. A so-called visual approach has been utilised. By means of a Product Family Master Plan, the content and scope of the platform have been modelled and visualised. This has contributed to commitment on the management and operational levels in the whole chain, from customer to production and delivery.