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Fernanda Troili

Researcher at Sapienza University of Rome

Publications -  10
Citations -  211

Fernanda Troili is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Dementia & Vascular dementia. The author has an hindex of 7, co-authored 10 publications receiving 123 citations.

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Emerging Biomarkers in Vascular Cognitive Impairment and Dementia: From Pathophysiological Pathways to Clinical Application.

TL;DR: Different biomarkers including the ones of inflammatory responses to central nervous system tissue injuries, of coagulation and thrombosis and of circulating microRNA are analysed to set different combinations of biomarkers to use for differential diagnosis among types of dementia.
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Perivascular Unit: This Must Be the Place. The Anatomical Crossroad Between the Immune, Vascular and Nervous System.

TL;DR: The “perivascular unit” is described as a key anatomical and functional substrate for the interaction between neuronal, immune and vascular mechanisms of brain injury, which are shared across different neurological diseases.
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Familial Alzheimer's disease sustained by presenilin 2 mutations: systematic review of literature and genotype-phenotype correlation.

TL;DR: Overall, the mutations involving the PSEN2 gene represent an extremely rare cause of FAD, having been reported to date in less than 200 cases, and are mainly associated, despite some peculiar and heterogeneous features, to a typical AD phenotype.
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Neurocognitive Assessment and Retinal Thickness Alterations in Alzheimer Disease: Is There a Correlation?

TL;DR: The results suggest that correlations between retinal thinning and cognitive performance warrant further investigation, and OCT can show early thickness changes in AD patients with subtle memory disturbances.
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Restless Legs Syndrome in a Group of Patients With Alzheimer’s Disease :

TL;DR: RLS appeared to be associated with neuropsychiatric symptoms such as apathy and RLS and apathy might share a common pathophysiological basis represented by a dysfunction of the central dopaminergic system.