A Recent Development in Alzheimer’s Research

Alzheimer’s Research

A new discovery that could revolutionize Alzheimer’s disease diagnosis and treatment was recently made by a group of South Korean scientists led by Director C. Justin LEE of the Institute for Basic Science’s Center for Cognition and Sociality.

The team demonstrated a mechanism by which the brain’s astrocytes become hazardous reactive astrocytes when they absorb elevated levels of acetates. They then, at that point, continued further to foster another imaging procedure that exploits this instrument to notice the astrocyte-neuron communications straightforwardly.

Alzheimer’s Advancement

Neuroinflammation in the brain is known to be associated with Alzheimer’s disease (AD), one of the main causes of dementia. Even though traditional neuroscience has long held the belief that amyloid beta plaques are to blame, treatments that target these plaques have not been able to treat or halt the disease’s progression.

In this most recent examination, Lee’s group utilized positron discharge tomography (PET) imaging with radioactive acetic acid derivation and glucose tests (11C-acetic acid derivation and 18F-FDG) to envision the progressions in neuronal digestion in Promotion patients.

“This study demonstrates significant academic and clinical value by directly visualizing reactive astrocytes, which have recently been highlighted as a primary cause of AD,” stated Dr. NAM Min-Ho, one of the first authors of this paper.

It was discovered that when amyloid-beta, a well-known toxin protein in AD, is present, increased acetate, which uptake is linked with reactive astrogliosis and raises aberrant astrocytic GABA synthesis.

The analysts showed that PET imaging with 11C-acetic acid derivation and 18F-FDG can be utilized to picture the responsive astrocyte-prompted acetic acid derivation hypermetabolism and related neuronal glucose hypometabolism in the minds with neuroinflammation and Promotion.

Also, when the scientists hindered receptive astrogliosis and astrocytic MCT1 articulation in the Promotion mouse model, they had the option to turn around these metabolic changes.

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