There are signs from past years to suggest that Alzheimer's disease is a reversible condition, at least in its earlier stages. In other words, that there is little loss of the structures holding the data of the mind, and the condition degrades the operation of the mind, not its underpinnings. The consensus, however, is that this stops being the case further into the progression of the disease, and significant losses do in fact occur. The researchers here disagree with that consensus, providing data to suggest that even in later stages the condition is not destroying significant numbers of synapses. This will definitely require further supporting evidence before it can be taken at face value, particularly since it is really only assessing the presence of key synaptic proteins in tissue samples, rather than any more in-depth analysis of structure and function.
Frequently encountered in the elderly, Alzheimer's is considered a neurodegenerative disease, which means that it is accompanied by a significant, progressive loss of neurons and their nerve endings, or synapses. A new study now challenges this view. Conducted among more than 170 subjects at various stages of Alzheimer's disease, the study has shown instead that the disease is accompanied by a minor decline in neuronal and synaptic markers. "Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects' prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer's disease. This is a radical change in thinking."
The scientists also attempted to correlate all these minor synaptic losses with the subjects' level of dementia. Their results show that the declines in synaptic biomarkers had little impact on the participants' cognitive skills. The study implicitly suggests that dementia is associated with a synaptic dysfunction rather than the disappearance of synapses from the patient's cortex. Identifying this dysfunction could lead to the development of effective treatments for this disease. "Until now, therapeutic interventions have been aimed at slowing synaptic destruction. Based on our study, we are going to have to change our therapeutic approach."