Abstract
Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer’s disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropathological hallmarks are amyloid-β (Aβ) plaques and neurofibrillary tangles. In the brain of AD patients and in mouse models of AD several morphological and functional changes, such as microgliosis and astrogliosis around Aβ plaques, as well as dendritic and synaptic alterations, are associated with these lesions. In this review article, we will summarize the current literature on synapse loss in mouse models of AD and discuss current and prospective treatments for AD.
Highlights
Synapse loss has harmful effects on cellular communication, leading to network disruption in the central nervous system (CNS)
Soluble oligomers extracted from Alzheimer’s disease (AD) brains disrupt long-term potentiation (LTP) and synaptic function in vitro and impair cognition when injected into healthy mice in vivo (Walsh et al, 2002; Cleary et al, 2005; Shankar et al, 2007)
These data indicate that pathways responsible for synaptic pruning during development are activated in AD that eventually lead to synapse loss (Stephan et al, 2012; Hong et al, 2016)
Summary
Synapse loss has harmful effects on cellular communication, leading to network disruption in the central nervous system (CNS). In vivo imaging studies revealed a loss of dendritic spines around plaques as a result of altered structural plasticity (Spires et al, 2005), whereas increased spine density and synaptic markers were obtained upon the removal of soluble oligomers (Spires-Jones et al, 2009). Together, these results support the idea that soluble forms of Aβ are toxic to synapses. The overexpression of mutant P301L in rTg4510 mice led to altered synaptic function and synapse loss (Crimins et al, 2011)
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