Saving Brain Connections by Targeting Synaptic Proteins May Treat Alzheimer’s, Study Finds

Saving Brain Connections by Targeting Synaptic Proteins May Treat Alzheimer’s, Study Finds
Proteins in nerve cell synapses, which transmit signals between neurons, are abnormal in the brains of patients with Alzheimer’s disease and other dementias, Swedish researchers concluded after performing a large-scale analysis of synaptic proteins in patients’ brains. By studying these flaws, researchers could distinguish between Alzheimer's patients and those with Parkinson’s disease dementia. A loss of synapses is tightly linked to cognitive decline in dementia. Therefore, the research team at Karolinska Institutet thinks that it may be possible to design treatments that prevent this loss by targeting the identified proteins — thereby preventing or slowing cognitive loss. Their study, “Synaptic markers of cognitive decline in neurodegenerative diseases: a proteomic approach,” appeared in the journal Brain. It included 32 patients who had died from Alzheimer’s, Parkinson’s disease with dementia, and dementia with Lewy bodies, as well as older adults without dementia. Researchers studied the prefrontal cortex — a brain region heavily involved in cognition. The team performed a so-called proteomic analysis, comparing proteins in the brains of patients and healthy people. They identified 10,325 proteins, of which 851 had functions within synapses. Among these, they pinpointed 25 proteins that were found in either higher or lower than normal amounts. They then validated these changes on a larger group of 92 brain samples. They noted that the levels of a handful of prote
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    The issue here, is are these proteins the cause or a result of Alzheimer’s disease? While their value as markers seems to be high, the issue of being therapeutic targets would need confirmation that they are involved in causing the disease.

  2. From what I have studied, the protein (amyloid) is produced naturally in the body and serves a purpose in keeping the synapses from firing uncontrollably, so as to prevent events like epilepsy. Amyloid can cause its own problems if it is allowed to accumulate unchecked. So there are certain components such as microglia that clear away excess amyloid. For reasons not clearly understood, sometimes microglia fails to clear away excess amyloid, and some processes stimulate the production of abnormal amounts of amyloid. When amyloid is allowed to accumulate in the brain, it disrupts normal synaptic functions, and this is one of the hallmarks of Alzheimer’s Disease.

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