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Monica Garcia-Alloza

Researcher at University of Cádiz

Publications -  75
Citations -  6358

Monica Garcia-Alloza is an academic researcher from University of Cádiz. The author has contributed to research in topics: Senile plaques & Alzheimer's disease. The author has an hindex of 34, co-authored 71 publications receiving 5469 citations. Previous affiliations of Monica Garcia-Alloza include University of Navarra & Harvard University.

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Rapid appearance and local toxicity of amyloid-beta plaques in a mouse model of Alzheimer's disease.

TL;DR: It is shown that plaques form extraordinarily quickly, Within 1–2 days of a new plaque’s appearance, microglia are activated and recruited to the site, leading to increasingly dysmorphic neurites over the next days to weeks, establishing plaques as a critical mediator of neuritic pathology.
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Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques

TL;DR: In this article, the authors used array tomography (AT) to quantify synapse loss in Alzheimer's disease and found that senile plaques are surrounded by a halo of oligomeric forms of amyloid beta.
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Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease

TL;DR: The consistent and early onset of beta-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying beta-AMyloid deposition, as well as exploring new therapeutic treatments.
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Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model.

TL;DR: Data suggest that curcumin reverses existing amyloid pathology and associated neurotoxicity in a mouse model of AD, which could lead to more effective clinical therapies for the prevention of oxidative stress, inflammation and neurotoxicity associated with AD.
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Cholinergic-serotonergic imbalance contributes to cognitive and behavioral symptoms in Alzheimer's disease

TL;DR: An imbalance between cholinergic-serotonergic systems may be responsible for the cognitive impairment associated to AD, and the relationships between neurochemical markers of both cholinesterase and serotonin systems and non-cognitive behavioral disturbances in patients with dementia are found.