Abstract β-amyloid is hypothesized to harm neural function and cognitive abilities by
perturbing synaptic transmission and plasticity in Alzheimer's disease (AD). To assess the …

The physiological function of amyloid precursor protein (APP) and its two homologues APP-
like protein 1 (APLP1) and 2 (APLP2) is largely unknown. Previous work suggests that lack …

Progressive cognitive decline in Alzheimer's disease could either be caused by a spreading
molecular pathology or by an initially focal pathology that causes aberrant neuronal activity …

Sleep, in addition to its brain restorative processes, plays an important role in memory
transfer from its temporary store in the hippocampus to the more permanent storage in the …

Alzheimer's disease (AD) is associated with aberrant neuronal activity, which is believed to
critically determine disease symptoms. How these activity alterations emerge, how stable …

The synaptic changes underlying the onset of cognitive impairment in Alzheimer's disease
(AD) are poorly understood. In contrast to the well documented inhibition of long-term …

The physiological role of the amyloid-precursor protein (APP) is insufficiently understood.
Recent work has implicated APP in the regulation of synaptic plasticity. Substantial evidence …

Impairment of episodic memory, a class of memory for spatiotemporal context of an event, is
an early symptom of Alzheimer's disease. Both spatial and temporal information are …

Alterations of brain network activity are observable in Alzheimer's disease (AD) together with
the occurrence of mild cognitive impairment, before overt pathology. However, in humans as …

Transgenic mice are used to model increased brain amyloid-β (Aβ) and amyloid plaque
formation reflecting Alzheimer's disease pathology. In our study hippocampal network …