Using scientific research to eradicate oblivion | a selection of papers on World Alzheimer's Day

Life Sciences

Life science

There are about 50 million Alzheimer's patients in the world, of which there are more than 10 million patients in
China.

September 21 is World Alzheimer's Day, and in order to raise public awareness of the disease and promote related research, we have selected Alzheimer's disease-related research papers from Cell, Neuron, Developmental Cell and Cell Reports from Cell Press's journal series, including chaperone-mediated autophagy Autophagy, CMA), Tau protein lesions and nucleoplasmic transport, microglia proliferation and β amyloid accumulation and other organic research, but also includes transcriptomics and genetic sequencing, 3D cell models, neurological disease imaging and other methodological applications and breakthroughs
.

It is hoped that through scientific research, the early screening and diagnosis
of Alzheimer's disease will be realized as soon as possible.

CMA prevents transferable neuronal proteome collapse

Academics believe that dysfunction of the components of the proteostasis network during aging, as well as a decline in protein quality control in neurons, promote neurodegeneration
.

Chaperone-mediated autophagy (CMA) is a selective autophagy that has been shown to degrade proteins
associated with neurodegeneration.

Mathieu Bourdenx, Evripidis Gavathiotis, and Ana Maria Cuervo from the Albert Einstein College of Medicine in the United States published a research paper at Cell examining the role of
CMA in neuronal protein homeostasis.

Using a mouse model with systemic and neuron-specific CMA blocking, the researchers demonstrated that the loss of neuronal CMA causes changes in neuronal function, selective changes in neuronal transferable proteomes, and protein toxicity, all of which are reminiscent of brain aging
.

Applying CMA loss on a mouse model of Alzheimer's disease has a synergistic negative effect on the proteome at risk of aggregation, thereby increasing susceptibility to neuronal disease and accelerating disease progression
.

Conversely, the use of chemical enhancement of CMA can improve the pathological condition of two different experimental mouse models of Alzheimer's disease
.

The study concluded that the proper functioning of CMA maintains a higher risk of proteome subset than general proteomic misfolding and is critical
for neuronal protein stability.

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