Alzheimer’s disease link
The new studies look at the connection between Alzheimer’s and the way brain cells regulate the amount of calcium they contain.
In order to stay healthy, brain cells need to maintain just the right amount of calcium at any given moment. That depends on the cells responding to signals from elsewhere in the brain.
Foskett and others say an abnormal response to these signals leads to abnormal calcium levels in brain cells, which ultimately leads to Alzheimer’s.
One of the new studies appears to confirm the link between calcium and Alzheimer’s. It identifies a gene linked to both Alzheimer’s and the calcium balance in brain cells.
The study’s lead author, Philippe Marambaud of Albert Einstein Medical College in New York, says scientists have been able to discover which chemicals in the brain are produced by the gene.
“So we have potentially not only identified a new risk factor, but also a gene product that could be targeted for drug discovery and therapy,” Marambaud says.
He says future drugs might be designed to correct abnormal calcium levels in brain cells. So far, efforts to treat Alzheimer’s have focused on preventing or eliminating the buildup of amyloid.
The second study suggests how an imbalance in calcium might actually cause Alzheimer’s.
Researchers looked at brain cells from people who have a rare, inherited form of the disease that can strike before the age of 40. They found that these people carry genes that not only cause amyloid buildup, but also problems with calcium regulation.
Calcium supplements
Take your calcium and magnesium supplement before a high fat meal of beef and/or dairy. Iron cancels the absorption of calcium. Vitamin D, magnesium and zinc help in the absorption of calcium.
The calcium in most supplements is either in the form of calcium carbonate or calcium citrate. Research shows that they are absorbed equally well with meals, but calcium carbonate is harder to digest than calcium citrate. People are usually advised to take calcium carbonate with or soon after a meal. Calcium citrate can be taken at any time.
Vitamin D. Getting enough vitamin D may be the most important variable in preventing osteoporosis. Vitamin D’s main function in the body is to aid calcium absorption. An analysis of data from the Nurses’ Health Study found that study participants who consume 500 IU of vitamin D daily are 37% less likely to have broken a hip than women who consume 140 IU. (IU stands for International Units, a measure of biological activity.) Neither total calcium nor milk consumption was associated with a lower risk for hip fracture.
The current FDA recommendation (the Daily Value) is 400 IU daily. Studies have shown that up to 50% of older Americans don’t get enough vitamin D. There are several reasons for this. The vitamin’s biologically active form is metabolized when the skin is exposed to the ultraviolet radiation in sunlight. Theoretically, sun exposure can give you all the vitamin D you need. But north of about 40 degrees latitude — the latitude of Philadelphia, Indianapolis, and Denver — the winter sunlight is too weak to produce significant amounts of vitamin D. Even in sunnier climes and times of year, older people tend to spend a lot of time indoors. Moreover, older skin is less effective in making the vitamin even when it’s exposed to sunlight. Sunscreens are another problem: they filter out much of the ultraviolet radiation that produces vitamin D.
Theoretically, you could make up for a shortage of sunshine-generated vitamin D with diet. The problem is that precious few foods contain the vitamin. For practical purposes, it’s limited to several types of saltwater fish. So decades ago, health officials in many northern countries decided to fortify foods with vitamin D. In the United States, milk — but not other dairy foods — was chosen. An 8-ounce glass of milk is supposed to contain 100 IU, although surveys have shown that the actual amount can be a great deal less.
Vitamin K. Your bones also need vitamin K, which is found in green, leafy vegetables.
… and the DON’Ts
Caffeine. If you’ve got a four-or-more cups-a-day coffee habit, cut back for the sake of your bones. High levels of caffeine may stimulate calcium excretion.
Protein. High levels of protein, especially animal protein, alter blood chemistry so calcium leaches out of your bones. But there is no cutoff here, just a general word of caution.
Vitamin A. Several studies have shown a correlation between high vitamin A intake and fracture risk. Some experts say it’s time to stop fortifying milk and breakfast cereal with vitamin A, because the population is getting older and the prevalence of osteoporosis is increasing. Meanwhile, you should avoid multivitamins that contain 10,000 IU of vitamin A, which is twice the recommended daily intake of 5,000 IU — and many experts think that’s too much. Bear in mind that the beta carotene in carrots and other vegetables is not a problem. It is far less biologically active than retinol, the form of vitamin A in many vitamin pills and fortified foods.
Homeostatis, Sodium and Potassium and Calcium
Activation of the neuron induces transient fluctuations in [Ca2+]i. This transient rise in [Ca2+]i is dependent on calcium entry via calcium channels and release of calcium from intracellular stores, finally resulting in increase in calcium levels, which activates calcium regulatory proteins to restore the resting calcium levels by binding to the calcium-binding proteins, sequestration into the endoplasmic reticulum and the mitochondria, and finally extrusion of calcium spike potential from the cell by adenosine triphosphate-driven Ca2+ pumps and the Na+/Ca2+ exchanger.
Improper regulation of calcium signaling, sequentially, likely contributes to synaptic dysfunction and excitotoxic and/or apoptotic death of the vulnerable neuronal populations. The cognitive decline associated with normal aging is not only due to neuronal loss, but is fairly the result of synaptic connectivity.
Many evidences support that Ca2+ dyshomeostasis is implicated in normal brain aging. Thus the chief factor associated with Alzheimer’s disease was found to be increase in the levels of free intracellular calcium, demonstrating that the excessive levels might lead to cell death, which provides a key target for the calcium channel blockers might be used as the neuroprotective agents in Alzheimer’s disease.