Abstract
Perturbed neuronal calcium homeostasis is a prominent feature in Alzheimer's disease (AD). Mitochondria accumulate calcium ions (Ca2+) for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell. Excessive Ca2+uptake into mitochondria often leads to mitochondrial membrane permeabilization and induction of apoptosis. Ca2+is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria. This review critically discusses the potential of manipulating mitochondrial Ca2+concentrations as a novel therapeutic opportunity for treating AD. This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca2+transport pathways. It is reasoned that these mitochondrial Ca2+modulators are most effective in combination with agents that increase the Ca2+buffering capacity of mitochondria. Modulation of mitochondrial Ca2+handling is a potential pharmacological target for future development of AD treatments.
| Original language | English |
|---|---|
| Pages (from-to) | 447-456 |
| Number of pages | 10 |
| Journal | Ageing Research Reviews |
| Volume | 9 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 1 Oct 2010 |
| Externally published | Yes |
Keywords
- Alzheimer's disease
- Calcium
- Mitochondria
- Mitochondrial membrane potential
- Voltage dependent anion channel
ASJC Scopus subject areas
- Biotechnology
- Biochemistry
- Ageing
- Molecular Biology
- Neurology