A Neurotransmission Gene May Help With Early AD Detection

Beacon Transcript – A neurotransmission gene may determine an earlier Alzheimer’s Disease diagnostic and treatment methods and maybe even possibly halt its progression.

The new study was carried out by a team of Tel Aviv University Sackler School of Medicine and was published in the Translational Psychiatry journal.

The researchers turned their attention towards and discovered a gene coding which could contribute to the detection of Alzheimer’s disease or AD. The protein gene coding could potentially turn of the neurotransmission signaling of AD.

RGS2 or Regulator of Protein Signaling 2 is a neurotransmission gene which has been linked, through this study, for the first time with AD.

The research reports show that a lower expression of this respective neurotransmission gene may increase an AD patient’s sensitivity to amyloid and its toxic effect.

Dr. David Gurwitz is one of the study’s lead authors and a Tel Aviv Sackler School of Medicine member of the Department of Human Molecular Genetics and Biochemistry.

Dr. Gurwitz went to explain the factors which led the research in this before unexplored direction. Previous Alzheimer’s Disease studies have, until now, established two pathological hallmarks which are specific to the neurodegenerative disease.

The two are the misfolded deposits of amyloid peptide plaques and also neurofibrillary tangles made of phosphorylated tau protein which were located in diseased brains.

But further studies have shown that the amyloid peptides could also be found in healthy older brains. As they were trying to determine the said peptide’s exact role in the AD pathology, the researchers started analyzing previous gene expression databases.

Thus, they found a common suspect in all AD cases, the RGS2 neurotransmission gene.

Further studies of the neurotransmission gene led to the conclusion that reduced RGS2 expression levels are signs of the early phases of the disease.

Their new proposal states that whether or not amyloid plaques are AD’s main culprits, the neuroprotective mechanism they activate lead to changes in the RGS2.

The researchers also advanced their neurotransmission gene theory and pointed out a new factor which might influence the disease.

According to them, the gene’s reduced expression levels increase neuron susceptibility to the possibly damaging effects of the amyloid peptides.

The team found that even in mild cognitive impairment cases, or the earliest phase of AD, RGS2 was already showing reduced expression levels.

Dr. Gurwitz pointed out the team’s belief that the reduced neurotransmission gene levels may well be a protective mechanism.

They consider that by lowering the transmission levels, the brain is trying to protect itself from the ongoing neurodegeneration characteristic of the disease.

Still, the protection measure presents benefits, but also increase the dangers. As the brain functions with fewer neurons, amyloid peptides neurotoxicity also increases. As such, misfolded amyloid plaques start to accumulate and increase in numbers.

The lead author stated that their study’s find will have to be further tested by other researchers, but that they may also introduce new detection and treatment methods.

Such a new treatment would try to diminish the negative effects of the reduced expression levels of the RGS2.

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