The cause of Alzheimer's disease is associated with a decrease in the amount of a protein that has been hypothesized to regulate the level of free calcium in brain cells, according to research conducted at the University of Medicine and Dentistry of New Jersey (UMDNJ) in Newark.
The studies show that Alzheimer's patients have markedly decreased levels of the calcium-bonding protein, CalbindinD28k, which may regulate the amount of calcium allowed to accumulate in the nerve cells of the brain. Without adequate amounts of this protein, calcium slowly accumulates, reaches toxic levels and, eventually, kills the cells.
This information suggests possible treatment therapies for Alzheimer's patients, possibly increasing the calcium-bonding capacity of a neuron cell to offset the vulnerability to Alzheimer's-type degeneration.
Researchers examined postmortem brain tissue of five patients with Alzheimer's disease and five patients who did not have Alzheimer's disease when they died. The examinations found that the brain tissue of all five Alzheimer's disease patients had lower levels of CaIbindin-D28k compared with those not having Alzheimer's disease. The difference between the two groups was as much as 80%.
The protein decrease was found to be due to a reduction in the expression of the gene that codes for the protein. It is unknown why this occurs in some people and not in others.
The decrease of the protein ties in with two other research areas relative to Alzheimer's disease. One is that a protein called beta amyloid accumulates in the brain and destroys nerve cells. This theory may be linked to this study because the formation of beta amyloid is thought to depend on calcium-mediated enzymes.
The other theory is that the cytoskel eton of nerve cells breaks down and ceases to work. Cytoskeletons are calcium-dependent and their breakdown could be triggered by the excess calcium, resulting from the lack of Calbindin-D28k.
For more information, contact Tom Slater, UMDNJ, News Service, 30 Bergen Street, Newark, NJ 07107-3007; 201-456-7276.