Abstract
Accumulation of amyloid beta (Aβ) in the brain in Alzheimer disease drives pathophysiology. A study in this issue of PLOS Biology revealed that Aβ from the liver can promote brain pathology, supporting that peripheral Aβ can contribute to neurodegeneration.
Highlights
Alzheimer disease is the most common type of dementia, and it is characterized by the presence of amyloid plaques in the brain that are comprised of aggregated amyloid beta (Aβ) peptides
The Aβ peptide is a fragment of the larger integral membrane protein called amyloid precursor protein (APP) that is expressed in neurons of the brain
When APP is cleaved by β and ɣ secretase enzymes, the resulting Aβ peptides form small soluble aggregates that induce toxicity in the brain and neuronal dysfunction followed by the deposition of Aβ peptides into insoluble amyloid plaques
Summary
Alzheimer disease is the most common type of dementia, and it is characterized by the presence of amyloid plaques in the brain that are comprised of aggregated amyloid beta (Aβ) peptides. Lam and colleagues have generated a new transgenic mouse with expression of human mutant APP primarily in the liver to investigate whether peripheral production of Aβ is sufficient to promote neurodegenerative phenotypes in the brain (Fig 1) [4]. Higher levels of Aβ peptide isoforms were found in the blood of individuals with pathological Aβ accumulation in brain and cognitive impairment [2].
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