New Study Reveals The Brain’s Protective Mechanism Against Alzheimer’s

“Buildups of “clumpy” proteins in the brain are well-known hallmarks of Alzheimer’s, but not everyone who has them goes on to develop this neurodegenerative disease. Why is that? New research investigates.”

Researchers know that bunches of a protein named “tau” and plaques of beta-amyloid indicate precursors of the Alzheimer’s disease. However, between 30 and 50 percent of those who have these clusters do not develop Alzheimer’s symptoms such as dementia during their lifetime.

Why does this occur? Research conducted by the University of Alabama at Birmingham reveals an answer: “dendritic spines.” Dendritic spines are the “doorknob-shaped” parts of the neuron that are involved in connection and sending information to other neurons.

A new study prompts researchers to think these “neuronal subunits” shield the brain against Alzheimer’s. Jeremy Herskowitz, Ph.D, who is an assistant professor at the University of Alabama at Birmingham’s Department of Neurology in the School of Medicine, led the research.

Herskowitz explains, “One obvious culprit in Alzheimer’s disease is the loss of dendritic spines and thus the loss of synapses […] This would impair the ability to think, so the assumption has been that those without dementia had healthy spines and those with dementia did not.”

Herskowitz adds that no one had researched to verify if this was true. With that, he assembled a team and completed a study to find the answer.

Their discoveries were officially published in the journal “Annals of Neurology” with Benjamin D. Boros being the first author of the paper.

Dendritic spines’ relation to Alzheimer’s

To determine that dendritic spines protected the brain from the onset of Alzheimer’s symptoms, Herskowitz and his team began comparing the dendritic structures of 21 patients who had Alzheimer’s to those of eight control groups who had Alzheimer’s prevalent brain pathologies but exhibited no symptoms, and those of 12 controls that had no pathologies nor Alzheimer’s disease. Patients were chosen from the memory clinics located at Emory University in Atlanta, Georgia.

Through bright-field microscopy, Herskowitz and the team created several images of the dendritic spines. Once completed, the used the images to create a 3-D digital reconstruction of the structures.

“We first noted that the control group had more dendritic spines than the group with Alzheimer’s, which matched beautifully with existing historical data,” Herskowitz said while explaining the research conclusions.

“But we also saw,” he continues, “that the group with Alzheimer’s pathology but no disease also had more spines than the Alzheimer’s group. In fact, they had roughly the same spine density as the control group.”

“But,” Prof. Herskowitz notes, “no one had gone in to see if that was true.” Therefore, he and his team set out to investigate.

“What is even more exciting,” adds Prof. Herskowitz, “is that the ‘pathology but no disease’ group had very long spines, longer than both the control group and the disease group.”

This could be “why some people are cognitively resilient to Alzheimer’s disease, even if they possess the typical Alzheimer’s pathology,” explains Prof. Herskowitz.

In their paper, Boros and colleagues conclude:

“These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD [Alzheimer’s disease] pathology from developing dementia.”

Read the full article here.