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Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex

Author(s): Olajide OJ; Chapman CA;

The hippocampus and entorhinal cortex (EC) accumulate amyloid beta peptides (Aß) that promote neuropathology in Alzheimer's disease, but the early effects of Aß on excitatory synaptic transmission in the EC have not been well characterized. To assess the acute effects of Aß1-42 on glutamatergic synapses, acute brain slices from wildtype rats were expo ...

Article GUID: 34144329


Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.

Author(s): Olajide OJ, Suvanto ME, Chapman CA

The entorhinal cortex (EC) is a vital component of the medial temporal lobe, and its contributions to cognitive processes and memory formation are supported through its extensive interconnections with the hippocampal formation. During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurod ...

Article GUID: 33495355


Hippocampal Degeneration and Behavioral Impairment During Alzheimer-Like Pathogenesis Involves Glutamate Excitotoxicity.

Author(s): Olajide OJ, Gbadamosi IT, Yawson EO, Arogundade T, Lewu FS, Ogunrinola KY, Adigun OO, Bamisi O, Lambe E, Arietarhire LO, Oluyomi OO, Idowu OK, Kareem R, Asogwa NT, Adeniyi PA

The hallmarks of Alzheimer's disease (AD) pathology include senile plaques accumulation and neurofibrillary tangles, which is thought to underlie synaptic failure. Recent evidence however supports that synaptic failure in AD may instead be instigated by enhanced N-methyl-D-aspartate (NMDA) ac ...

Article GUID: 33420680


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