Related Experiment Video
Updated: May 7, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
Can the calcium hypothesis explain synaptic loss in Alzheimer's disease?
Elena Popugaeva1, Ilya Bezprozvanny
1Laboratory of Molecular Neurodegeneration, St. Petersburg State Polytechnical University, St. Petersburg, Russia.
Abstract:
Alzheimer's disease (AD) is the threat of modern humankind that is provoked by increased human lifespan. Despite extensive studies on AD pathology for more than 100 years, there are no disease-preventing therapies. Growing evidence suggests the role of calcium (Ca2+) in the pathogenesis of AD. The main purpose of the article is to understand whether modern science is able to explain the synapse loss observed in early AD and discuss the role of Ca2+ hypothesis in it. Based on results obtained in our laboratory and others, we propose that familial AD-associated mutations in presenilins cause a Ca2+ overload of endoplasmic reticulum stores which leads to compensatory downregulation of the neuronal store-operated Ca2+ (nSOC) entry pathway. We propose that synaptic nSOC is necessary for the stability of mature synaptic spines and that dysfunction of this pathway may play an important role in synaptic and memory loss in AD.
Related Concept Videos
Alzheimer Disease ll: Pathophysiology
Long-term Depression
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease l: Introduction
Dementia l: Introduction

