Gunnar K. Gouras

ORCID iD
orcid.org/0000-0002-5500-6325
  • Country
Sweden

Sources:
Gunnar K. Gouras (2016-01-24)

  • Keywords
Alzheimer's disease, amyloid

Sources:
Gunnar K. Gouras (2015-07-13)

  • Email
gkgouras@gmail.com

Sources:
(2013-05-06)

  • Other IDs
Scopus Author ID: 6701650128

Sources:
Scopus to ORCID (2013-05-06)

Biography

Gunnar Keppler Gouras (Gunnar K. Gouras in papers) is Professor of Experimental Neurology, head of the Neurobiology section and the Experimental Dementia Research Unit, and coordinator of the Strategic Research Environment in Neuroscience - MultiPark, in the Department of Experimental Medical Science, Faculty of Medicine, Lund University in Lund, Sweden. His research group focuses on Alzheimer's disease and related neurodegenerative disorders. Prior to his move to Lund in 2011, he was Professor of Neurology and Neuroscience at Weill Medical College of Cornell University. His research has focused on the intracellular and synaptic biology of Alzheimer's disease-linked beta-amyloid. Beta-amyloid was traditionally viewed as an extracellular peptide that abnormally aggregates as amyloid plaques in Alzheimer's disease. His publication Gouras GK et al., 2000, provided the first evidence that particularly the disease-linked Abeta42 variant accumulates early within vulnerable neurons in Alzheimer's disease, as well as in Down syndrome, a disorder that is also characterised by age-related amyloid pathology and dementia. Utilising immuno-electron microscopy his group subsequently discovered that Abeta42 localises to multivesicular bodies of normal neurons and with Alzheimer's disease preferentially accumulates and aggregates in synaptic terminals, providing the 1st physical link between beta-amyloid and synapses (Takahashi RH et al., 2002; 2004); as well as the 1st association of beta-amyloid promoting tau pathology in synaptic terminals (Takahashi RH et al., 2010). His lab further provided the first evidence for selective beta-amyloid dependent alterations in synaptic proteins (Almeida CG et al., 2005) via inhibiting the ubiquitin proteasome system (Almeida CG et al., 2006), and the surprising finding that antibodies directed against beta-amyloid require internalisation into cells to protect against alterations in synapses (Tampellini D et al., 2007). More recent work focused on effects of synaptic activity on cellular beta-amyloid metabolism and synapse pathology (Tampellini D et al., 2009; 2010; 2011).
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