INVESTIGATING SECONDARY EFFECTS OF BACE1 INHIBITION, A PROMISING THERAPY FOR ALZHEIMER'S DISEASE
Grant number: 1058672 | Funding period: 2014 - 2016
Synapses transfer information between neurons in the brain. In Alzheimer’s disease (AD), synapse loss results in dementia therefore it is imperative that any potential therapeutic drugs do not inadvertently cause further synapse loss. Drugs aimed at blocking production of toxic protein fragments in AD might have adverse secondary effects on synapse development and function. This research will determine whether this is the case and inform new therapeutic approaches aimed at minimizing side effects.
Related publications (9)
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Martina Pigoni, Hung-En Hsia, Jana Hartmann, Jasenka Rudan Njavro, Merav D Shmueli, Stephan A Mueller, Gokhan Guener, Johanna Tueshaus, Peer-Hendrik Kuhn, Rohit Kumar, Pan Gao, Mai Ly Tran, Bulat Ramazanov, Birgit Blank, Agnes L Hipgrave Ederveen, Julia Von Blume, Christophe Mulle, Jenny M Gunnersen, Manfred Wuhrer, Gerhard Rammes
Seizure protein 6 (SEZ6) is required for the development and maintenance of the nervous system, is a major substrate of the protea..
Lack of Sez6 Family Proteins Impairs Motor Functions, Short-Term Memory, and Cognitive Flexibility and Alters Dendritic Spine Properties
Amelia Nash, Timothy D Aumann, Martina Pigoni, Stefan F Lichtenthaler, Hiroshi Takeshima, Kathryn M Munro, Jenny M Gunnersen
Seizure-related gene 6 (Sez6), Sez6-Like (Sez6L), and Sez6-Like 2 (Sez6L2) comprise a family of homologous proteins widely express..
Beta-Site Amyloid Precursor Protein Cleaving Enzyme 1 Inhibition Impairs Synaptic Plasticity via Seizure Protein 6
Kaichuan Zhu, Xianyuan Xiang, Severin Filser, Petar Marinkovic, Mario M Dorostkar, Sophie Crux, Ulf Neumann, Derya R Shimshek, Gerhard Rammes, Christian Haass, Stefan F Lichtenthaler, Jenny M Gunnersen, Jochen Herms
BACKGROUND: Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is a promising drug target for the treatment of Alzheime..
Functions of the Alzheimer's Disease Protease BACE1 at the Synapse in the Central Nervous System
Kathryn M Munro, Amelia Nash, Martina Pigoni, Stefan F Lichtenthaler, Jenny M Gunnersen
Inhibition of the protease β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) is a promising treatment strategy for Alzhei..
Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons
Martina Pigoni, Johanna Wanngren, Peer-Hendrik Kuhn, Kathryn M Munro, Jenny M Gunnersen, Hiroshi Takeshima, Regina Feederle, Iryna Voytyuk, Bart De Strooper, Mikail D Levasseur, Brian J Hrupka, Stephan A Mueller, Stefan F Lichtenthaler
BACKGROUND: The protease BACE1 (beta-site APP cleaving enzyme) is a major drug target in Alzheimer's disease. However, BACE1 thera..
The HSA21 gene EURL/C21ORF91 controls neurogenesis within the cerebral cortex and is implicated in the pathogenesis of Down Syndrome
Shan Shan Li, Zhengdong Qu, Matilda Haas, Ngo Linh, You Jeong Heo, Hyo Jung Kang, Joanne Maria Britto, Hayley Daniella Cullen, Hannah Kate Vanyai, Seong-Seng Tan, Tailoi Chan-Ling, Jenny Margaret Gunnersen, Julian Ik-Tsen Heng
Copy number variations to chromosome 21 (HSA21) cause intellectual disability and Down Syndrome, but our understanding of the HSA2..