HIV-associated neurocognitive disorders involve extracellular Nef-induced modification of lipid rafts and redistribution of Alzheimer’s disease-related proteins

Mechanisms of Neurodegeneration: Protein aggregation and failure of autophagy

Probiotics and exercise can slow Alzheimer’s progression by altering composition of gut bacteria

Losing memory: Toxicity from mutant APP and amyloid beta explain the hippocampal neuronal damage in Alzheimer's disease

Lysosomal Dysfunction is Linked to Exosomal Secretion

Immunity’s flipside: Microglia promote Alzheimer’s pathology during inflammation

The Proteasome and Autophagy Pathways in Alzheimer's Disease

The neurodegenerative disorder, Alzheimer's disease, is responsible for 60 to 80% of all dementia cases.1   Neurodegeneration occurs in response to the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau.

The C99 fragment of amyloid precursor protein (APP)

Alzheimer’s Disease (AD) is a neurodegenerative disorder that is characterized by an abundance of the beta-amyloid peptide in the brain.  When AD was first discovered, it was determined that beta-amyloid was produced as a result of the proteolysis of the amyloid precursor protein (APP).  Aside from its role in AD, the single-pass transmembrane APP has a high expression level in the brain and tends to concentrate at the synapses of neurons.  Because of this localization, it has been suggested that APP plays a role in synapse formation and potentially plasticity.  However, the

Beta Amyloid (MOAB2) and the link between traumatic brain injury and Alzheimer’s disease

An epidemiological association between traumatic brain injury (TBI) and Alzheimer's disease (AD) has long been established.  Interestingly, an increase in beta amyloid  (one hallmark of AD) directly following TBI has been observed.  In fact, it has been reported that with a greater level of TBI comes a higher risk of developing AD, or other neurodegenerative disorders, in the future.  Roberts et al first presented research that beta amyloid plaques found in TBI patients are very similar to those found in AD patients.

Niemann Pick-C1 and cholesterol dynamics

Niemann-Pick type C1 (NPC1) mediates low-density cholesterol transport from late endosomes and lysosomes to other areas of the cell via receptor mediation endocytosis.  Although cholesterol moves freely inside the cell, it cannot independently export out of the lysosome, which is where NPC1 steps in.