Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 60, Issue 3, Pages 289-297Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-016-0826-4
Keywords
Alzheimer's; Autophagy; Calcium; Copper; Presenilin; Trafficking; Zinc
Categories
Funding
- Operational Infrastructure Support Grant
- Australian National Health and Medical Research Council (NHMRC)
- Australian Research Council (ARC)
- NHMRC Dementia Research Fellowship
Ask authors/readers for more resources
An imbalance in metal homeostasis is a prominent feature of Alzheimer's disease (AD). A wealth of evidence from independent studies over the past two and half decades has found changes to the distribution of brain iron, zinc, and copper in AD patients and animal models of the disease. Early research focused on the association of these metals with amyloid beta (A beta), particularly extraneuronal A beta plaque pathology. In contrast, there are numerous studies that have demonstrated a loss of iron-, zinc-, or copper-dependent cellular functions in AD animal and cell models, highlighting the importance of metal homeostasis in maintaining healthy brain function. Characterizing the molecular pathways that are impacted by iron, zinc, or copper will shed light on how these metals affect neuoroprotection, and conversely, neurodegeneration. Of particular interest is the role that the AD-associated presenilins have on protein trafficking and degradation, as metal homeostasis is dependent on the efficient trafficking and recycling of specific metal transporters. This review summarizes what is currently known about presenilin-dependent protein trafficking and the role of presenilin in protein turnover, particularly via the autophagy-lysosomal system.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available