Mobile Digital Health

~ by Damion Drilla

Dementia isn’t all about aging, studies show. Health in mid-life can have a marked effect on cognitive ability later on.

A British study of 10,308 people, mostly men, followed the subjects from roughly the ages of 35-55 (the study started in 1985) to about 60-75 years (the study ended in 2004).

Coronary heart disease in midlife was found to be linked to lower cognition in later years. In men, heart disease was linked to lower reason, vocabulary, and MMSE scores. In women, it corresponded additionally to lower phonemic and semantic fluency.

The longer the heart disease – meaning, the earlier it was contracted – the greater the drop in cognitive ability over the years. This suggests that heart disease creates an ongoing condition that continuously deteriorates mental function until dementia kicks in.

~ by Cher Giovani

The study wasn’t about dementia: it was about blood pressure. A British group researching hypertension in the elderly followed a group of participants aged 80 and over to record the effects of drug therapy treatment for hypertension on the patients. Among the many variables measured was cognitive impairment.

The 3,336 subjects were randomly assigned to receive or not receive drug therapy for hypertension. At the beginning, they were all screened to have similar medical records, including no diagnosis of dementia.

The study found that treatment definitely reduced incidence of stroke, heart failure, and death. There were also 263 cases of dementia, including vascular dementia, Alzheimer’s, and ordinary cognitive decline. Treatment showed a small, but definite increase in cognitive decline among the untreated subjects.

Further study would be necessary to see if treating hypertension directly affects dementia, or if the reduced decline is tied to the form of treatment itself; the greatest reduction in dementia was found with the use of calcium channel blockers.

By Stan Readley

It’s long been known that beta amyloid, a disruptive plaque substance, forms on the brain as Alzheimer’s disease progresses. What is not known is if the plaque causes the disease, or is caused by it. Particularly confusing: some people have beta amyloid in their brain and no Alzheimer’s disease.

Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School led a study that collected beta amyloid samples from cadavers donated to science and injected them into the brains of mice. Surprisingly, not all the mice developed Alzheimers. Only the mice who received a particular strain of beta amyloid developed the neurological disease. The two-molecule, soluble beta-amyloid seems to clog the synapses and disrupt communication between sections of the brain.

The study seems to directly inculpate a single form of beta amyloid as the cause of Alzheimers. If further studies corroborate these findings, we could be on the way to discovering the cause and cure for the degenerative neurological disease.