Federica Angiulli


Bachelor of Science in Medical and Pharmaceutical Biotechnologies (2013) and Master of Science in Medical Biotechnologies and Molecular Medicine (2015) from University of Bari.

Recipient of the Rotary Global Grant Scholarship in 2017 –Disease Prevention and Treatment area of focus, for the project “Molecular mechanisms of cerebrovascular amyloidosis in Alzheimer’s disease and related disorders”.

Research Scholar in Dr. Silvia Fossati lab – Department of Psychiatry, NYU School of Medicine (New York University, USA) in 2017, working on the Effect of Carbonic Anhydrase Inhibitors Methazolamide and Acetazolamide on murine models of Alzheimer’s Disease. The collaboration with Dr. Fossati continues in 2018 for the project “Identification of brain-derived diagnostic biomarkers for TBI and PTSD in blood and other biological fluids”, using the SIMOA technology.

From March 2018, Visiting Researcher in Dr. Fabrizio Piazza’s CAA and AD Translational Research and Biomarkers Lab at University of Milano Bicocca for the project “biomarkARIA”, and member of the Inflammatory Cerebral Amyloid Angiopathy and Alzheimer’s Disease Biomarkers (iCAB) International Network.

From November 2018, PhD student in Experimental Neurosciences at the University of Milano Bicocca under Professor Carlo Ferrarese supervision.

From January to May 2020, Visiting PhD student in Dr. Silvia Fossati lab – Alzheimer’s Center, Lewis Katz School of Medicine at Temple University (Philadelpia, USA) – applying the SIMOA technology to the project “CSF and Plasma Biomarkers of ARIA in Patients With Cerebral Amyloid Angiopathy-Related Inflammation”. 


Neuroinflammation in the pathogenesis of Alzheimer’s disease: role of peripheral monocytes

  • Track: Neuroscienze Sperimentali
  • Tutor: Carlo Ferrarese

Alzheimer’s disease (AD), the most common cause of dementia, is an age-related neurodegenerative disorder characterized by progressive cognitive deterioration, affecting both memory and other aspects of cognitive functioning. Despite being well established that neurofibrillary tangles and β-amyloid (Aβ) plaques play a central role in the development of the disease, it is now recognized that neuroinflammation contributes to AD pathogenesis just as much as its pathological hallmarks. The peripheral immune system has long been considered completely separated from the central nervous system by means of the blood brain barrier (BBB). In AD however, because of the BBB dysfunction, blood-derived macrophages are recruited into the brain and can be found within the core of amyloid plaques; here they mature a specific immune reaction towards Aβ and develop a phagocytic phenotype. 

In light of these premises, the specific aim of this PhD project is to investigate the mechanisms involved in Aβ-induced chemotaxis of peripheral monocytes in the context of AD pathology, and to elucidate their putative role in Aβ clearance and disease progression.