Newly Found Proteins May Explain Alzheimer’s Devastating Effects

Newly Found Proteins May Explain Alzheimer’s Devastating Effects

Despite decades of research, pinpointing the exact cause of brain damage in Alzheimer's disease has proven challenging. A team from Emory University in the US may have found a crucial piece of the puzzle.
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Despite decades of research, pinpointing the exact cause of brain damage in Alzheimer’s disease has proven challenging. A team from Emory University in the US may have found a crucial piece of the puzzle.

Reevaluating Amyloid Beta’s Role in Alzheimer’s

Much research has investigated amyloid beta plaques in Alzheimer’s, but some now view them as a byproduct rather than a cause of brain damage. Lab studies suggest these plaques don’t directly harm brain cells, and treatments targeting them have fallen short, leaving key aspects of the disease unclear.

The latest findings suggest other factors may be at play. Emory biochemists Yona Levites, Eric Dammer, and their team found that proteins accumulating with amyloid beta plaques might cause Alzheimer’s symptoms like confusion, communication issues, and memory loss.

The researchers compared protein combinations in Alzheimer’s mouse models and human subjects—some with Alzheimer’s, others with plaques but no symptoms. They identified over 20 proteins that accumulated with amyloid beta in both. Many are signaling molecules that, when trapped in plaques, may trigger harmful brain processes.

Emory biochemist Todd Golde suggested that proteins beyond amyloid beta might drive Alzheimer’s brain damage. The team linked amyloid beta plaques to increased levels of midkine and pleiotrophin, which are associated with inflammation. These proteins could be targets for new therapies.

Inflammatory Proteins in Alzheimer’s Brain Damage

Amyloid beta’s role as a scaffold for other proteins might explain conflicting study results. The team observed that amyloid naturally supports other mechanisms. Initial lab tests revealed that midkine and pleiotrophin accelerated plaque formation.

Levites and her team suggest that protein accumulation in plaques may be part of the brain’s response to amyloid beta, potentially helping to clear or neutralize the toxic amyloid structure.

Protective or Harmful Response?

This suggests other molecules may affect whether amyloid beta proteins cause neuronal damage. Researchers haven’t ruled out other theories, like Alzheimer’s as an autoimmune disease, and stress that more research is needed to understand Alzheimer’s complex brain changes.


Read the original article on: Science Alert

Read more: New Compound Restores Memory Function in Alzheimer’s Cases

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