Clare E. Wallace
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View article: Heterozygosity of lysosomal enzyme genes and Alzheimer's disease
Heterozygosity of lysosomal enzyme genes and Alzheimer's disease Open
Background Although lysosome dysfunction has been implicated in Alzheimer's disease (AD), it is unclear what level or type of dysfunction is pathogenic. We hypothesize that haploinsufficiency of lysosomal enzymes is associated with AD and …
View article: Haploinsufficiency of lysosomal enzyme genes in Alzheimer’s disease
Haploinsufficiency of lysosomal enzyme genes in Alzheimer’s disease Open
There is growing evidence suggesting that the lysosome or lysosome dysfunction is associated with Alzheimer’s disease (AD). Pathway analysis of post mortem brain-derived proteomic data from AD patients shows that the lysosomal system is pe…
View article: Phospholipase D3 drives microglial response to amyloid pathology in Alzheimer’s disease
Phospholipase D3 drives microglial response to amyloid pathology in Alzheimer’s disease Open
Background Amyloid‐beta (Aβ) plaque formation is a well‐established hallmark for Alzheimer’s disease (AD). However, the processes behind plaque formation are not understood. Previous work from our group identified rare coding variants for …
View article: Sex-dependent effects of acute stress on amyloid-β in male and female mice
Sex-dependent effects of acute stress on amyloid-β in male and female mice Open
The risk of developing Alzheimer’s disease is mediated by a combination of genetics and environmental factors, such as stress, sleep abnormalities and traumatic brain injury. Women are at a higher risk of developing Alzheimer’s disease tha…
View article: Phospholipase D3 contributes to Alzheimer’s disease risk via disruption of Aβ clearance and microglia response to amyloid plaques
Phospholipase D3 contributes to Alzheimer’s disease risk via disruption of Aβ clearance and microglia response to amyloid plaques Open
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain. AD is also the result of complex genetic architecture that can be leveraged to understand pathways central to…
View article: Pimavanserin, a 5HT<sub>2A</sub> receptor inverse agonist, rapidly suppresses Aβ production and related pathology in a mouse model of Alzheimer’s disease
Pimavanserin, a 5HT<sub>2A</sub> receptor inverse agonist, rapidly suppresses Aβ production and related pathology in a mouse model of Alzheimer’s disease Open
Amyloid‐β (Aβ) peptide aggregation into soluble oligomers and insoluble plaques is a precipitating event in the pathogenesis of Alzheimer's disease (AD). Given that synaptic activity can regulate Aβ generation, we postulated that 5HT 2A ‐R…
View article: Effect of escitalopram on Aβ levels and plaque load in an Alzheimer mouse model
Effect of escitalopram on Aβ levels and plaque load in an Alzheimer mouse model Open
Escitalopram significantly reduced Aβ in mice, similar to previous findings in humans treated with acute dosing of an SSRI.
View article: Combination anti-Aβ treatment maximizes cognitive recovery and rebalances mTOR signaling in APP mice
Combination anti-Aβ treatment maximizes cognitive recovery and rebalances mTOR signaling in APP mice Open
Drug development for Alzheimer’s disease has endeavored to lower amyloid β (Aβ) by either blocking production or promoting clearance. The benefit of combining these approaches has been examined in mouse models and shown to improve patholog…
View article: Rapid in vivo measurement of β-amyloid reveals biphasic clearance kinetics in an Alzheimer’s mouse model
Rapid in vivo measurement of β-amyloid reveals biphasic clearance kinetics in an Alzheimer’s mouse model Open
Findings from genetic, animal model, and human studies support the observation that accumulation of the β-amyloid (Aβ) peptide in the brain plays a central role in the pathogenic cascade of Alzheimer’s disease (AD). Human studies suggest t…