Is Alzheimer's Disease dipped in a Molecular Loss of Motivation?

Is Alzheimer's Disease dipped in a Molecular Loss of Motivation? ...

Preventing memory loss, researchers from theIndiana University School of Medicine are looking at why neuropsychiatric symptoms, such as apathy and irritability, occur in most Alzheimers disease patients.

According toYao-Ying Ma, MD, and an assistant professor of pharmacology and toxicology, the study has been reimagined in the publication Molecular Psychiatry. Researchers identified a receptor in the brain that results in a loss of neurons and synaptic structure when used in an Alzheimers disease model.

The nucleus accumbens, a critical brain region, is not studied much by Alzheimers disease scientists; it''s mostly explored to understand motivational and emotional processes. Previous studies have shown that the volume of nucleus accumbens, like the cortical and hippocampal regions in the brain, is reduced in adults with Alzheimers disease.

Ma, a relatively new author of Alzheimers disease research, has a background in drug addiction research and synaptic communication. These are some of the neuropsychiatric symptoms commonly diagnosed with substance abuseapathy, mood swings, and anxiety.

A significant number of Alzheimers patients have started showing mood swings even before the introduction of cognitive deficiencies, and they have a greater chance to develop symptoms of depression, according to Ma.

These neuropsychiatric symptoms may appear later than memory loss, but no effective treatments are available, according to Ma. This study examined the effect of synaptic calcium permeable receptors (CP-AMPARs) in the nucleus accumbens in an Alzheimers disease model. This process is linked to an accumulation of calcium that can be fatal to the neuron by forming a positive feedback mechanism.

This synaptic loss in the brain causes motivation limitations. Ma said that targeting these receptors in the brain and blocking them might prevent or delay the formation of Alzheimers disease associated neuropsychiatric disorders and ultimately cognitive difficulties.

If we can postpone the pathological progression in one of the affected areas, such as the nucleus accumbens, Ma said, then this might be the result of other pathological changes in the future.

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