Amyloid Precursor Protein and Alzheimer’s Disease

TL;DR

Alzheimer’s disease involves the buildup of harmful proteins like amyloid beta and tau, and the amyloid precursor protein plays a key role in this process.

Contribution

The paper highlights the role of amyloid precursor protein in Alzheimer’s disease and identifies gaps in understanding its biogenesis.

Findings

Alzheimer’s disease is marked by amyloid beta and hyperphosphorylated tau accumulation.

APP can follow either a non-amyloidogenic or amyloidogenic pathway, influencing Aβ plaque formation.

The full process of APP biogenesis remains unclear and requires further research.

Abstract

Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders associated with age or inherited mutations. It is characterized by severe dementia in the late stages that affect memory, cognitive functions, and daily life overall. AD progression is linked to the accumulation of cytotoxic amyloid beta (Aβ) and hyperphosphorylated tau protein combined with other pathological features such as synaptic loss, defective energy metabolism, imbalances in protein, and metal homeostasis. Several treatment options for AD are under investigation, including antibody-based therapy and stem cell transplantation. Amyloid precursor protein (APP) is a membrane protein considered to play a main role in AD pathology. It is known that APP in physiological conditions follows a non-amyloidogenic pathway; however, it can proceed to an amyloidogenic scenario, which leads to the generation of extracellular deleterious Aβ plaques. Not all steps of APP biogenesis are clear so far, and these questions should be addressed in future studies. AD is a complex chronic disease with many factors that contribute to disease progression.

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