Background Identifying effective strategies to prevent memory loss in AD has eluded
researchers to date, and likely reflects insufficient understanding of early pathogenic …

The current state of the AD research field is highly dynamic is some respects, while
seemingly stagnant in others. Regarding the former, our current lack of understanding of …

Alzheimer's disease (AD)-linked presenilin (PS) mutations result in pronounced
endoplasmic reticulum calcium disruptions that occur before detectable histopathology and …

Short-term plasticity preserves a brief history of synaptic activity that is communicated to the
postsynaptic neuron. This is primarily regulated by a calcium signal initiated by voltage …

In the past years, major efforts have been made to understand the genetics and molecular
pathogenesis of Alzheimer's disease (AD), which has been translated into extensive …

Neurotransmitter release from presynaptic terminals is primarily regulated by rapid Ca2+
influx through membrane-resident voltage-gated Ca2+ channels (VGCCs). Moreover …

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by abnormal
accumulation of β-amyloid and tau and synapse dysfunction in memory-related neural …

Work from the past 40 years has unraveled a wealth of information on the cellular and
molecular mechanisms underlying synaptic plasticity and their relevance in physiological …

Background Excessive synaptic loss is thought to be one of the earliest events in
Alzheimer's disease (AD). However, the key mechanisms that maintain plasticity of synapses …

Presenilin mutations result in exaggerated endoplasmic reticulum (ER) calcium release in
cellular and animal models of Alzheimer's disease (AD). In this study, we examined whether …