#radial

LIPID RAFTS/CHOLESTEROL

amyloid-beta peptides are formed when APP undergoes proteolysis (protein breakdown) in the cholesterol-rich lipid rafts. (An area in the plasma membrane dense with sphingolipids + cholesterol, leading the organisation of signalling molecules and their compartmentalisation)

Cleavage (or proteolysis) of APP in other regions of the membrane, prevents the formulation of toxic amyloid beta.

As a result, differences in the structure of the membrane of the individual may affect amyloid beta production, and the progression of Alzheimer's as a result.

AMYLOID BETA PEPTIDES -> AMYLOID PLAQUES

Accumulation of amyloid beta outside cells form amyloid plaques. These characterise Alzheimer's disease in patients.

Additionally, aggregation of abnormally-phosphorylated tau proteins into intraneuronal neurofibrillary tangles is another key characteristic of the disease.

This second paragraph may be harder to understand, so I will be breaking it down; to phosphorylate means to add a Phosphate to a molecule. This is an essential process in biology, and I would recommend learning further about it.

Tau normally stables microtubules in the brain, preventing breakdown. These microtubules are important for neuronal structure and intercellular (between cells) transport.

Excessive or abnormal phosphorylation of tau proteins leads to a "tangle formation" and oligomerisation (where small monomers link together to form a larger chain.) This leads to microtubule destabilisation.