BACE1

Phospholipid regulation in cognitive impairment and vascular dementia

An imbalance in lipid metabolism in neurodegeneration is still poorly understood. Phospholipids (PLs) have multifactorial participation in vascular dementia as Alzheimer, post-stroke dementia, CADASIL between others. Which include the hyperactivation of phospholipases, mitochondrial stress, peroxisomal dysfunction and irregular fatty acid composition triggering proinflammation in a very early stage of cognitive impairment. The reestablishment of physiological conditions of cholesterol, sphingolipids, phospholipids and others are an interesting therapeutic target to reduce the progression of AD. We propose the positive effect of BACE1 silencing produces a balance of phospholipid profile in desaturase enzymes-depending mode to reduce the inflammation response, and recover the cognitive function in an Alzheimer´s animal and brain stroke models. Pointing out there is a great need for new well-designed research focused in preventing phospholipids imbalance, and their consequent energy metabolism impairment, pro-inflammation and enzymatic over-processing, which would help to prevent unhealthy aging and AD progression.

New small molecule labelling tools to investigate the physiological functions of beta-Secretase BACE1

The Neuronal Seizure Protein 6 (SEZ6) is a Substrate of the Alzheimer Protease BACE1 and a Ligand for the LDL-Related Protein 1 (LRP1)

NRF2 regulates BACE1 and BACE1-AS expression in a negative way

BACE1-dependent effects of IL-6 on cortical circuits

FENS Forum 2024