Abstract:
:Amyloid-beta (Abeta) deposition is a defining feature of Alzheimer's disease (AD). The toxicity of Abeta aggregation is thought to contribute to clinical deficits including progressive memory loss and cognitive dysfunction. Therefore, Abeta peptide has become the focus of many therapeutic approaches for the treatment of AD due to its central role in the development of neuropathology of AD. In the past decade, taking the advantage of multiphoton microscopy and molecular probes for amyloid peptide labeling, the dynamic progression of Abeta aggregation in amyloid plaques and cerebral amyloid angiopathy has been monitored in real time in transgenic mouse models of AD. Moreover, amyloid plaque-associated alterations in the brain including dendritic and synaptic abnormalities, changes of neuronal and astrocytic calcium homeostasis, microglial activation and recruitment in the plaque location have been extensively studied. These studies provide remarkable insight to understand the pathogenesis and pathogenicity of amyloid plaques in the context of AD. The ability to longitudinally image plaques and related structures facilitates the evaluation of therapeutic approaches targeting toward the clearance of plaques.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Dong J,Revilla-Sanchez R,Moss S,Haydon PGdoi
10.1016/j.neuropharm.2010.04.007subject
Has Abstractpub_date
2010-09-01 00:00:00pages
268-75issue
4-5eissn
0028-3908issn
1873-7064pii
S0028-3908(10)00109-7journal_volume
59pub_type
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