Browsing by Author "ROWAN, MICHAEL"
Now showing items 1-14 of 14
-
Amyloid Oligomers and Mature Fibrils Prepared from an Innocuous Protein Cause Diverging Cellular Death Mechanisms.
DAVEY, GAVIN; BOLAND, JOHN; ROWAN, MICHAEL (2015) -
Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory.
ROWAN, MICHAEL (2008)Alzheimer?s disease (AD) constitutes a rising threat to public health. Despite extensive research in cellular and animal models, identifying the pathogenic agent present in the human brain and showing that it confers key ... -
Beta-amyloid-mediated inhibition of NMDA receptor-dependent long-term potentiation induction involves activation of microglia and stimulation of inducible nitric oxide synthase and superoxide
ANWYL, ROGER; ROWAN, MICHAEL (2004)The mechanisms underlying the inhibition of long-term potentiation (LTP) induction by amyloid -peptide (A ) were investigated in the medial perforant path of the rat and mouse dentate gyrus in vitro . Evidence ... -
Interaction between prion protein and toxic amyloid ß assemblies can be therapeutically targeted at multiple sites.
KLYUBIN, IGOR; ROWAN, MICHAEL (2011)A role for PrP in the toxic effect of oligomeric forms of A?, implicated in Alzheimer's disease (AD), has been suggested but remains controversial. Here we show that PrP is required for the plasticity-impairing effects of ... -
MGlu5 receptors and cellular prion protein mediate amyloid-ß- facilitated synaptic long-term depression in vivo
ROWAN, MICHAEL (2014)NMDA-type glutamate receptors (NMDARs) are currently regarded as paramount in the potent and selective disruption of synaptic plasticity by Alzheimer's disease amyloid β-protein (Aβ). Non-NMDAR mechanisms remain relatively ... -
Neurotransmitter receptor and time dependence of the synaptic plasticity disrupting actions of Alzheimer's disease Aß in vivo.
ROWAN, MICHAEL (2014)Many endogenous factors influence the time course and extent of the detrimental effects of amyloid β-protein (Aβ) on synaptic function. Here, we assessed the impact of varying endogenous glutamatergic and cholinergic ... -
Peripheral administration of a humanized anti-PrP antibody blocks Alzheimer's disease Aß synaptotoxicity
ROWAN, MICHAEL (2014)Alzheimer's disease (AD) is associated with pathological assembly states of amyloid-β protein (Aβ). Aβ-related synaptotoxicity can be blocked by anti-prion protein (PrP) antibodies, potentially allowing therapeutic targeting ... -
Protection against ß-amyloid-induced synaptic and memory impairments via altering ß-amyloid assembly by bis(heptyl)-cognitin
ROWAN, MICHAEL; ANWYL, ROGER; ROWAN, MICHAEL JOSEPH; ANWYL, ROGER (2015)β-amyloid (Aβ) oligomers have been closely implicated in the pathogenesis of Alzheimer’s disease (AD). We found, for the first time, that bis(heptyl)-cognitin, a novel dimeric acetylcholinesterase (AChE) inhibitor derived ... -
Removal of Synaptic Ca2+-Permeable AMPA Receptors during Sleep.
ULRICH, DANIEL; ROWAN, MICHAEL (2011)here is accumulating evidence that sleep contributes to memory formation and learning, but the underlying cellular mechanisms are incompletely understood. To investigate the impact of sleep on excitatory synaptic transmission, ... -
Secreted amyloid ß-proteins in a cell culture model include N-terminally extended peptides that impair synaptic plasticity
ROWAN, MICHAEL (2014)Evidence for a central role of amyloid β-protein (Aβ) in the genesis of Alzheimer’s disease (AD) has led to advanced human trials of Aβ-lowering agents. The “amyloid hypothesis” of AD postulates deleterious effects of ...