The brain cells of AD patients are over-consuming resources that are vital to neurotransmission

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Alzheimer's disease (AD) is the most common type of dementia, which causes the death of neurons and causes the brain to shrink

A recent study conducted by a team from the School of Life Sciences at the Chinese University of Hong Kong showed that early changes in brain metabolism may explain neurodegeneration

These findings lay the foundation for the development of new and targeted nutrition-centric and disease-improving treatment strategies

Low-Density Lipoprotein Receptor-Related Protein 6 Cell Surface Availability Regulates Fuel Metabolism in Astrocytes.

A previous study showed that there is an association between a synonymous single nucleotide polymorphism (SNP) in the LRP6 gene and AD

This metabolic-dependent shift not only leads to impaired brain glycolysis, but also depletes amino acids that are essential for neurotransmitter circulation and synthesis

Metabolic changes affect people with genetic polymorphisms at the LRP6 locus and are also related to people with genetic variants in the apolipoprotein E (APOE) E4 allele, which is the most common genetic risk factor for AD [about 6.

Loss of LRP6 in astrocytes leads to astrocyte proliferation, leading to impaired synapses, neurodegeneration, cognitive and memory function in mice

As the latest progress in this field shows that brain metabolic dysfunction is the core of Alzheimer's disease, targeting the brain's new metabolic needs may become a potential strategy for managing disease progression

Specific nutritional supplements are not a new concept clinically

Depletion of these raw materials essential for neurotransmitter biosynthesis and recycling can lead to impaired synaptic, cognitive, and memory functions; prepare for the early changes often found in LOAD