Calcium, a trace mineral plays an important role in build and maintain
strong bones and teeth, found abundantly in meat, poultry, fish, nut,
seeds, bean, etc. As we age, calcium is absorbed less effectively.
8. Calcium and S100 proteins
S100 proteins play a crucial role in multiple important biological processes in vertebrate organisms acting predominantly as calcium
signal transmitters.According to the study by the Polish Academy of
Sciences, after four Ca(2+) ions bind, it undergoes a dramatic
conformational
change, resulting in exposure, in each of its two identical subunits, a
large hydrophobic cleft that binds to target proteins. It has been shown
that abnormal expression of S100A1 is strongly correlated with a number
of severe human diseases: cardiomyopathy and neurodegenerative
disorders(8).
9. Calcium and aluminum salt
Most humans living in industrialized societies are routinely exposed to
bioavailable aluminum salts in the form of additives-in
commercially-prepared foods, alum-clarified drinking water, certain
pharmaceuticals, sunscreens, and other topical applications. Minute
amounts of this aluminum are absorbed into the circulation. Trace
aluminum levels cross the blood-brain barrier and progressively
accumulate in large pyramidal neurons of the hippocampus, cortex, and
other brain regions vulnerable in Alzheimer's disease. According to the
study by the St George Hospital Campus, intraneuronal aluminum
interferes with Ca2+ metabolism in the aged brain
and describes a way to test this hypothesis. This paper reviews: 1)
major changes that occur in brain Ca2+ homeostasis and Ca2+ signaling,
subtly with aging and more overtly in Alzheimer's disease; and 2)
evidence from the scientific literature that aluminum causes these same
changes in neurons(9).
10. calcium
and aluminum in Neurodegenerative disorders
Both calcium
and aluminum have been implicated in the cell damage and death that
occurs in several neurodegenerative disorders including Alzheimer's
disease (AD). In the study to examine the effects of experimentally elevated intraneuronal levels of aluminum ([Al]i) and/or calcium
([Ca2+]i) on neuronal degeneration and antigenic alterations in the
microtubule-associated protein tau in cell cultures of rat hippocampus
and human cerebral cortex, showed that Exposure of cultures to Al3+ alone (200 microM) for up to 6 d did not
result in neuronal degeneration. Neurons exposed to the divalent cation
ionophore A23187 degenerated within 4 h when Ca2+ was present in the
culture medium whether or not Al3+ was present. Measurements of [Ca2+]i
using the calcium
indicator dye fura-2 demonstrated a direct relationship between
increased [Ca2+]i and neuronal degeneration. In contrast, neurons did
not degenerate when exposed to A23187 in the presence of Al3+ and the
absence of Ca2+, despite a 10-fold elevation in [Al]i as measured by
laser microprobe mass spectrometry. Calcium
influx, but not aluminum influx, elicited antigenic changes in tau
similar to those seen in AD neurofibrillary tangles. Neurons exposed to
glutamate in the presence of Al3+ but in the absence of Ca2+ were not
vulnerable to injury. Finally, increased [Al]i occurred in neurons that
degenerated as the result of exposure to glutamate indicating that
aluminum associates with degenerating neurons(10).
11. Neuronal calcium homeostasis in the aging nervous system
Maintenance of the cellular calcium
homeostasis plays an important role for neuronal cell function and
interneuronal cell to cell communication. Therefore, alterations of the
neuronal Ca2+ homeostasis may play a
crucial role for brain aging in general and for age-related deficits in
cognitive functions particularly.
Numerous studies indicate various disturbances of the Ca2+ homeostasis
on different levels like Ca2+ channel properties, 45Ca2+ uptake, or Ca2+
binding proteins. Investigations on alterations of the free
intracellular calcium
concentration ([Ca2+]i) in presynaptic synaptosomal preparations led to
inconsistent results reporting increased or unchanged [Ca2+]i in aged
animals, according to the Central Institute of Mental Health, Dept. Psychopharmacology(11).
12. Disruption of calcium homeostasis and Alzheimer's disease (AD)
Oligomerization, conformational changes, and the consequent
neurodegeneration of Alzheimer's β-amyloid protein (AβP) play crucial
roles in the pathogenesis of Alzheimer's disease (AD). Mounting evidence
suggests that oligomeric AβPs cause the disruption of calcium
homeostasis, eventually leading to neuronal death, according to the
School of Pharmaceutical Sciences, Kyushu University of Health and
Welfare(12).
13. BK Channels in Cardiovascular Diseases and Aging
Aging is a major risk factor for cardiovascular diseases, one of the
main world-wide causes of death. Several structural and functional
changes occur in the cardiovascular system during the aging process and
the mechanisms. BK channels are transmembrane proteins that play a key role in many
physiological processes, including regulation of vascular tone.In vascular smooth muscle cells,
BK opening and the consequent efflux of potassium (K(+)) leads to
membrane hyperpolarization, which is followed by the closure of
voltage-dependent Ca(2+) channels, reduction of Ca(2+) entry and
vasodilatation. BK regulates nitric oxide-mediated vasodilatation and
thus is crucial for normal endothelial function(13).
14. Ca(2+) waves regulate blood vessel tone and vasomotion
Agonist-stimulated smooth muscle Ca(2+)
waves regulate blood vessel tone and vasomotion.The Pharmacology, and
Therapeutics, University of British Columbia, present a first report of
endothelin-1 stimulated waves of Ca(2+) depletion from the sarcoplasmic
reticulum of vascular smooth muscle cells
using a calsequestrin-targeted Ca(2+) indicator and confirmed that
these waves are due to regenerative Ca(2+)-induced Ca(2+) release by the
receptors for inositol 1,4,5-trisphosphate(14).
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Sources
(8) http://www.ncbi.nlm.nih.gov/pubmed/23351007
(9) http://www.ncbi.nlm.nih.gov/pubmed/22330830
(10) http://www.ncbi.nlm.nih.gov/pubmed/8448655
(11) http://www.ncbi.nlm.nih.gov/pubmed/7997060
(12) http://www.ncbi.nlm.nih.gov/pubmed/21547225
(13) http://www.ncbi.nlm.nih.gov/pubmed/23423545
(14) http://www.ncbi.nlm.nih.gov/pubmed/23408969
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