Decrease In Bone Density May Be An Early Sign Of Alzheimer's Disease

Alzheimer's disease is one of those neurodegenerative disorders that do not have a clear cause at the moment. Experts say that fewer than 5 percent of cases of Alzheimer's disease have a clear genetic cause, making it hard to predict who will develop the devastating brain-wasting disorder. Now, with the help of a mouse model of Alzheimer's disease, researchers discover a link between early bone loss and brain degeneration.

According to NCBI, scientists are still trying to understand the complex, incurable -- and seemingly unstoppable -- changes that take place in the brain of people with Alzheimer's disease.

However, what they do know is this. Before the symptoms show, abnormal deposits of beta-amyloid and tau proteins are forming throughout the brain, gradually clogging up brain cells so they stop working and die. Because of this, it is vital to look for ways to identify and stop these early brain changes before they damage the brain

Reduced bone mineral density and the disease it leads to, osteoporosis, are much more common in people with Alzheimer's disease. The bone conditions often happen before the dementia symptoms are spotted. However, the underlying mechanisms linking them are still unclear.

The researchers in the new study had suspected that bone loss is an additional early symptom of Alzheimer's disease itself, due to abnormal production of serotonin, a brain chemical that controls mood and sleep, two processes that are also affected early in Alzheimer's disease, reported Medical News Today.

They conducted a series of investigations using "htau mice," mice genetically altered to have human forms of a type of tau protein, which becomes abnormal in Alzheimer's disease and disrupts an important internal cell structure called microtubules.

For the study, researchers measured bone mineral density in the htau mice before developing significant signs of tau abnormality. They found significant reduced bone mineral density compared with normal mice, especially in the males.

Furthermore, htau mice revealed major cell changes in a region of the brainstem known as the dorsal raphe nucleus (DRN), "a pivotal structure in the regulation of the adult skeleton," note the authors. The DRN also produces most of the brain's serotonin.

It is also important to note that the researchers found elevated levels of abnormal tau protein in the same area of the brain as early as four months of age in the htau mice.

They concluded that their findings reveal a reduced bone mineral density occurs earlier than the overt brain degeneration seen in a tau-based mouse model of Alzheimer's disease and that alterations in tau protein occur in the serotonin-producing cells of the brainstem of such mice

Now, the team thinks that further studies should look for the molecular mechanism that associates bone loss to a reduction in serotonin in early Alzheimer's disease in humans.

Lead author Christine Dengler-Crish, assistant professor of pharmaceutical sciences, and anatomy and neurobiology at NEOMED, suggests that "Measurement of bone density, which is routinely performed in the clinic, could serve as a useful biomarker for assessing AD [Alzheimer's disease] risk in our aging population."