Miguel Tábuas Pereira

Miguel Tábuas Pereira

Consultant Neurologist - Cohead of the Dementia Clinic

Centro Hospitalar e Universitário de Coimbra

Biography

Miguel is a cognitive neurologist and researcher at Centro Hospitalar e Universitário de Coimbra, where he is responsible for the Memory Clinic, a reference in Dementia Care in Portugal. His work is focused on degenerative dementia.

He is currently doing his PhD in the Genetic causes of Dementia under the mentoring of Prof. Isabel Santana (CHUC, PT), Rita Guerreiro (Van Andel Institute, MI, US) and Jose Bras (Van Andel Institute, MI, US).

Interests

  • Alzheimer’s Disease
  • Frontotemporal Dementia
  • Dementia with Lewy Bodies
  • Genetics
  • Biomarkers

Education

  • PhD - Neuroscience

    Faculty of Medicine of the University of Coimbra (ongoing)

  • PgDip - Clinical Neurology

    University College of London (ongoing)

  • Neurology Specialty (19.87)

    Centro Hospitalar e Universitário de Coimbra (2018)

  • Medicinae Doctor, MD (15.5)

    Faculty of Medicine, University of Coimbra (2011)

Skills

Clinical Neurology

100%

Genetics

80%

CSF Biomarkers

90%

Neuropsychology

90%

Statistics

80%

Thinking outside of the Box

150%

Experience

 
 
 
 
 

CONSULTANT NEUROLOGIST

Centro Hospitalar e Universitário de Coimbra

Oct 2018 – Dec 2020 Coimbra
Responsible for the Memory Clinic
 
 
 
 
 

MEMBER OF THE EDUCATION COMMITTEE

European Academy of Neurology

Oct 2017 – Dec 2021 Vienna
Residents and Research Fellows Representative
 
 
 
 
 

MEMBER OF THE HIGHER CORTICAL FUCNTIONS SCIENTIFIC PANEL

European Academy of Neurology

Oct 2017 – Dec 2021 Vienna
Residents and Research Fellows Representative

Recent Publications

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Faster Cortical Thinning and Surface Area Loss in Presymptomatic and Symptomatic C9orf72 Repeat Expansion Adult Carriers

C9orf72 mutation carriers have faster cortical thinning and surface loss throughout adulthood in regions that show atrophy in symptomatic subjects. This suggests that the pathogenic effects of the mutation lead to structural cerebral changes decades prior to symptoms.
Code DOI

Neuronal Pentraxin 2 - A Synapse-Derived CSF Biomarker in Genetic Frontotemporal Dementia

We conclude that NPTX2 is a promising synapse-derived disease progression biomarker in genetic FTD.
Code DOI

Headache Intensity Is Associated With Increased White Matter Lesion Burden in CADASIL Patients

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common hereditary cause of vascular dementia in adults. Age, female sex and headache intensity are associated with increased white matter lesion volume in CADASIL.
Code DOI

Plasma Glial Fibrillary Acidic Protein Is Raised in Progranulin-Associated Frontotemporal Dementia

Raised GFAP concentrations appear to be unique to GRN-related FTD, with levels potentially increasing just prior to symptom onset, suggesting that GFAP may be an important marker of proximity to onset, and helpful for forthcoming therapeutic prevention trials
Code DOI

Age at Symptom Onset and Death and Disease Duration in Genetic Frontotemporal Dementia - An International Retrospective Cohort Study

Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership.
Code DOI
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