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Dr. Danielle Andrade - University Health Network. Toronto, ON, CA

Dr. Danielle Andrade Dr. Danielle Andrade

Medical Director, Epilepsy Program; Director, Epilepsy Genetics Program; Director, Transition Epilepsy Program | University Health Network

Toronto, ON, CANADA

Dr. Danielle Andrade is a neurologist specialized in the areas of epilepsy and genetics






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A neurologist specialized in the areas of epilepsy and genetics, Dr. Andrade is the Medical Director of the Epilepsy Program and the founder and Director of the first Adult Epilepsy Genetics Program in Ontario. Dr. Andrade is also cross-appointed to the Hospital for Sick Children in Toronto, where she is the Director of the Transitional Epilepsy Program.

Industry Expertise (2)

Health and Wellness

Health Care - Services

Areas of Expertise (4)





Education (4)

Universidade Federal do Parana: MD, Medicine 1995

Universidade Federal do Parana: Post-Graduating Training, Neurology 1999

University of Toronto: MSc, Sciences 2004

University of Toronto: Fellowship, Epilepsy 2006

Affiliations (2)

  • Krembil Neuroscience Centre
  • Associate Professor Neurology University of Toronto

Languages (1)

  • English

Media Appearances (5)

Purple Day: Living With Genetically-Determined Epilepsy



It's not surprising that the Clozza family experienc​ed a magical moment on a recent trip to Disney World. But the reason ​went beyond daughter Daniela meeting an enchanted princess or two.

"It was very special for us because it was the first time we were able to travel as a family," said Guida Clozza, Daniela's mother. "I never thought we would be able to do something like this."

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Gene May Boost Death Risk for People With Mild Epilepsy

HealthDay  online


FRIDAY, Oct. 23, 2015 (HealthDay News) -- Researchers say they've identified a gene mutation that might increase the risk of sudden death in people with mild epilepsy.

The researchers studied a four-generation family with nine members who had epilepsy caused by a mutation of the DEPDC5 gene.

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Gene Associated With Sudden Unexpected Death In Epilepsy Discovered

Epilepsy Research UK  online


A new genetic discovery has opened the door for potential ways of screening patients for the risk of sudden unexpected death in epilepsy (SUDEP).

Published in the journal Neurology: Genetics, the study from Toronto’s Krembil Neuroscience Centre has discovered a gene mutation that increases the risk of SUDEP in patients with mild forms of the disease.

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How this epilepsy toolkit could help Canadian workplaces

Global News  online


TORONTO – National statistics on epilepsy suggest that about 0.6 per cent of the population has the condition. About 15,500 people per year are diagnosed – they could be your family, friends and coworkers.

But do you understand the mechanics behind epilepsy? Canadian experts created a new toolkit to shed light on the disorder for employers, human resources managers and colleagues. Their hope is their tools will remove the stigma behind a disorder that’s easily manageable.

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5 Things You Need To Know About Epilepsy

Huffington Post  online


It's easy to take for granted that the whole of our consciousness is rooted in nothing more than the complex activity of our brain cells. It's only when activity goes awry that the importance of our immaculately-tuned brain activity becomes obvious.

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Articles (5)

Dravet syndrome, lamotrigine, and personalized medicine Wiley Publishing


Lamotrigine (LTG) has an established place in our armamentarium of antiepileptic drugs (AEDs). As a broad spectrum AED, it is often used in patients with severe epilepsy, especially those with both focal and generalized onset seizures. Patients with Dravet syndrome would appear to be good candidates for treatment with LTG, since they have severe epilepsy and several types of seizures (including those with focal and generalized onset). However, some reports have shown that the majority of patients with Dravet syndrome have an increase in seizure frequency and/or severity when taking LTG.

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Practical guidelines for managing adults with 22q11.2 deletion syndrome nature.com


22q11.2 Deletion syndrome (22q11.2DS) is the most common microdeletion syndrome in humans, estimated to affect up to 1 in 2,000 live births. Major features of this multisystem condition include congenital anomalies, developmental delay, and an array of early- and later-onset medical and psychiatric disorders. Advances in pediatric care ensure a growing population of adults with 22q11.2DS. Informed by an international panel of multidisciplinary experts and a comprehensive review of the existing literature concerning adults, we present the first set of guidelines focused on managing the neuropsychiatric, endocrine, cardiovascular, reproductive, psychosocial, genetic counseling, and other issues that are the focus of attention in adults with 22q11.2DS. We propose practical strategies for the recognition, evaluation, surveillance, and management of the associated morbidities.

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Delineating the 15q13.3 microdeletion phenotype: a case series and comprehensive review of the literature nature.com


Recurrent 15q13.3 deletions are enriched in multiple neurodevelopmental conditions including intellectual disability, autism, epilepsy, and schizophrenia. However, the 15q13.3 microdeletion syndrome remains ill-defined.

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Biallelic Truncating Mutations in FMN2, Encoding the Actin-Regulatory Protein Formin 2, Cause Nonsyndromic Autosomal-Recessive Intellectual Disability Elsevier


Dendritic spines represent the major site of neuronal activity in the brain; they serve as the receiving point for neurotransmitters and undergo rapid activity-dependent morphological changes that correlate with learning and memory. Using a combination of homozygosity mapping and next-generation sequencing in two consanguineous families affected by nonsyndromic autosomal-recessive intellectual disability, we identified truncating mutations in formin 2 (FMN2), encoding a protein that belongs to the formin family of actin cytoskeleton nucleation factors and is highly expressed in the maturing brain. We found that FMN2 localizes to punctae along dendrites and that germline inactivation of mouse Fmn2 resulted in animals with decreased spine density; such mice were previously demonstrated to have a conditioned fear-learning defect. Furthermore, patient neural cells derived from induced pluripotent stem cells showed correlated decreased synaptic density. Thus, FMN2 mutations link intellectual disability either directly or indirectly to the regulation of actin-mediated synaptic spine density.

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A pilot double-blind trial using verapamil as adjuvant therapy for refractory seizures Elsevier

November 2014
Given verapamil's property as a glycoprotein inhibitor, this drug could increase the effective concentration of antiepileptic drugs (AEDs) in the epileptic foci, reducing the number of seizures. This pilot study was designed to evaluate the safety and efficacy of verapamil as adjunct therapy in pharmacoresistant patients with focal onset seizures.

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