Abstract
In summary, it seems that in many neurologic disorders - of both genetic and toxic origin - mitochondrial disruption leads to an altered calcium metabolism and thus to cell death. This raises the possibility that various protective agents, such as antioxidants, that improve mitochondrial function efficiency, may be of benefit in high risk individuals.
Original language | English |
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Pages (from-to) | 356-359 |
Number of pages | 4 |
Journal | Israel Medical Association Journal |
Volume | 6 |
Issue number | 6 |
State | Published - 2004 |
Bibliographical note
Cited By :1Export Date: 11 September 2022
CODEN: IMAJC
Correspondence Address: Rahamimoff, R.; Dept. of Physiology, , Jerusalem 91120, Israel; email: ramir@cc.huji.ac.il
Chemicals/CAS: 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine, 28289-54-5; adenine, 22177-51-1, 2922-28-3, 73-24-5; calcium ion, 14127-61-8; cyclosporin A, 59865-13-3, 63798-73-2; cytosine, 71-30-7; glutamic acid, 11070-68-1, 138-15-8, 56-86-0, 6899-05-4; guanine, 69257-39-2, 73-40-5; huntingtin, 191683-04-2; manganese, 16397-91-4, 7439-96-5; reduced nicotinamide adenine dinucleotide dehydrogenase, 9027-14-9, 9032-21-7, 9079-67-8; rotenone, 83-79-4; superoxide dismutase, 37294-21-6, 9016-01-7, 9054-89-1; calcium, 7440-70-2; Calcium, 7440-70-2
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Keywords
- Calcium
- Genetic disease
- Mitochondria
- Neurotoxicity
- Oxidative stress
- 1,2,3,6 tetrahydro 1 methyl 4 phenylpyridine
- adenine
- antioxidant
- calcium ion
- cyclosporin A
- cytosine
- glutamic acid
- guanine
- huntingtin
- manganese
- mitochondrial DNA
- phosphatidylinositol 3,4,5 trisphosphate
- reactive oxygen metabolite
- reduced nicotinamide adenine dinucleotide dehydrogenase
- rotenone
- superoxide dismutase
- calcium
- Alzheimer disease
- amyotrophic lateral sclerosis
- apoptosis
- autophagy
- calcium homeostasis
- calcium metabolism
- calcium signaling
- calcium transport
- cell death
- disorders of mitochondrial functions
- gene mutation
- high risk patient
- human
- Huntington chorea
- Leber hereditary optic neuropathy
- neurofibrillary tangle
- neurologic disease
- oxidative stress
- Parkinson disease
- point mutation
- review
- senile plaque
- transport kinetics
- trinucleotide repeat
- metabolism
- nerve cell
- pathophysiology
- physiology
- Alzheimer Disease
- Amyotrophic Lateral Sclerosis
- Humans
- Huntington Disease
- Mitochondrial Diseases
- Neurons
- Optic Atrophy, Hereditary, Leber
- Parkinson Disease