Calcium dysregulation, and lithium treatment to forestall Alzheimer's disease – a merging of hypotheses
Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca2+ in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca2+ may forestall c...
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| Published in | Cell calcium (Edinburgh) Vol. 55; no. 3; pp. 175 - 181 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier Ltd
01.03.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca2+ in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca2+ may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca2+ concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca2+ levels are N-methyl-d-aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca2+ through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca2+ levels. |
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| AbstractList | Intracellular Ca(2+) concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca(2+) in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca(2+) may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca(2+) concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca(2+) levels are N-methyl-d-aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca(2+) through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca(2+) levels.Intracellular Ca(2+) concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca(2+) in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca(2+) may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca(2+) concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca(2+) levels are N-methyl-d-aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca(2+) through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca(2+) levels. Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca2+ in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca2+ may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca2+ concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca2+ levels are N-methyl-d-aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca2+ through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca2+ levels. Intracellular Ca(2+) concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca(2+) in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca(2+) may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca(2+) concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca(2+) levels are N-methyl-d-aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca(2+) through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca(2+) levels. Abstract Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role of dysregulated intracellular Ca2+ in Alzheimer's disease had led to the hypothesis that controlling intracellular Ca2+ may forestall cognitive decline. Lithium has been shown to reduce intracellular Ca2+ concentrations. Two well-characterized neuronal targets of lithium that may affect intracellular Ca2+ levels are N-methyl- d -aspartate (NMDA) receptors and inositol monophosphatase (IMP). Results from a recent single-center placebo-controlled randomized trial suggest that long-term lithium treatment at subtherapeutic doses may have the potential to delay the progression of disease, and observational studies have shown that lithium reduces the prevalence of dementia in subjects with bipolar disorder on long-term lithium therapy. I am advancing the hypothesis that lithium may protect against cognitive decline by stabilizing intracellular Ca2+ through a dual, synergistic mechanism of targeting both extracellular and intracellular sites, via antagonizing NMDA-receptors and inhibiting IMP. Insights derived from this hypothesis could lead to an improved understanding of the molecular pathology of Alzheimer's disease, and have implications on the evaluation and use of therapeutics that alter intracellular Ca2+ levels. |
| Author | Wallace, James |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24636273$$D View this record in MEDLINE/PubMed |
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| Keywords | Lithium Inositol trisphosphate Inositol monophosphatase Congestive heart failure Inclusion body myositis Digoxin Alzheimer's disease NMDA-receptors |
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| Snippet | Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative role... Abstract Intracellular Ca2+ concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The... Intracellular Ca(2+) concentrations are tightly regulated, and elevated levels sustained over periods of time can cause cellular deterioration. The putative... |
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| SubjectTerms | Advanced Basic Science Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Calcium - metabolism Calcium Signaling - drug effects Congestive heart failure Inclusion body myositis Digoxin Glycogen Synthase Kinase 3 - antagonists & inhibitors Glycogen Synthase Kinase 3 - metabolism Humans Inositol monophosphatase Inositol trisphosphate Lithium Lithium - pharmacology Lithium - therapeutic use Models, Theoretical Neuronal Plasticity NMDA-receptors Phosphoric Monoester Hydrolases - antagonists & inhibitors Phosphoric Monoester Hydrolases - metabolism Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Receptors, N-Methyl-D-Aspartate - metabolism |
| Title | Calcium dysregulation, and lithium treatment to forestall Alzheimer's disease – a merging of hypotheses |
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