Isabel Ferreira, MD

Hospital Prof. Doutor Fernando Fonseca, Amadora

isabelferreira

Isabel Amorim Ferreira finished the Medicine course at Faculdade de Medicina de Lisboa in 2008. She attended the Training Course of Palliative Care in the same year. In 2009 she obtained a post-graduation in Hospital Emergency, being currently a resident internal doctor at Hospital Prof. Doutor Fernando Fonseca in Amadora, since the 1st of January 2010. She attended boarding school at Hospital Curry Cabral, Lisbon, in the service of Medicine II.

She is a member of CEDOC - FCM/UNL since 2011. In 2012 she concluded her Master's degree in Clinical Research both at Faculdade de Ciências Médicas de Lisboa and at Northeastern University, in Boston.

She has published several scientific communications, being the first author of some of these.


HUMORAL RESPONSE IN THE PATHOGENESIS OF ALZHEIMER'S DISEASE

Alzheimer’s disease (AD) is the most common form of dementia worldwide and its prevalence is expected to double by the year 2050. The precise mechanisms responsible for AD are unknown but the histopathologic features are well-characterised. The most compelling hypothesis for neuronal loss and cognitive decline in AD is the amyloid cascade hypothesis, which states that AD is the result of amyloid beta (AB) overproduction and/or ineffective clearance and its accumulation in the brain would be the critical step in AD pathogenesis. Currently, identification of proteins that bind AB and modulate its aggregation and neurotoxicity could provide the basis for novel treatment approaches. Apolipoprotein (ApoA-I), the main constituent of human HDL,  interacts with the extracellular domain of amyloid precursor protein (APP), as well as with AB itself. Epidemiological studies have shown a marked decrease of plasma ApoA-I levels in AD patients, with an inverse correlation between the ApoA-I level and the risk of AD. Our group is currently investigating if anti-ApoA-I antibodies may prevent the formation of the AD/ApoA-I complex and by doing so blocking the protective effect of ApoA-I in AD. We base the hypothesis on the possibility that patients with AD might have anti-ApoA-I antibodies in plasma and that these can interfere with the complex formation in the CSF.