Diseases caused by the aggregation of proteins are known as proteopathies, and they are primarily caused by aggregates in the following structures:
cytosol, e.g. Parkinsons and Huntingtons
nucleus, e.g. Spinocerebellar ataxia type 1 (SCA1)
endoplasmic reticulum (ER), (as seen with neuroserpin mutations that cause familial encephalopathy with neuroserpin inclusion bodies)
extracellularly excreted proteins, amyloid-beta in Alzheimers diseaseThere are two main avenues eukaryotic cells use to remove troublesome proteins or organelles:

ubiquitin–proteasome: protein ubiquitin along with enzymes is key for the degradation of many proteins that cause proteopathies including polyQ expansions and alpha-synucleins. Research indicates proteasome enzymes may not be able to correctly cleave these irregular proteins, which could possibly result in a more toxic species. This is the primary route cells use to degrade proteins.Decreased proteasome activity is consistent with models in which intracellular protein aggregates form. It is still unknown whether or not these aggregates are a cause or a result of neurodegeneration. autophagy–lysosome pathways: a form of programmed cell death (PCD), this becomes the favorable route when a protein is aggregate-prone meaning it is a poor proteasome substrate. This can be split into two forms of autophagy: macroautophagy and chaperone-mediated autophagy (CMA).macroautophagy is involved with nutrient recycling of macromolecules under conditions of starvation, certain apoptotic pathways, and if absent, leads to the formation of ubiquinated inclusions. Experiments in mice with neuronally confined macroautophagy-gene knockouts develop intraneuronal aggregates leading to neurodegeneration. chaperone-mediated autophagy defects may also lead to neurodegeneration.
In free fatty acid form, the chemical structure of stearidonic acid is:

Examples
Polyunsaturated fatty acids with 16- and 18-carbon chains are sometimes classified as short chain polyunsaturated fatty acids (SC-PUFA), as opposed to long-chain polyunsaturated fatty acids (LC-PUFA), which have more than 18 carbon atoms.Both the essential fatty acids are SC-PUFA with an 18-carbon chain:

ω-3 fatty acid:
α-linolenic acid or ALA (18:3n-3)
ω-6 fatty acid:
linoleic acid or LA (18:2n-6)These two fatty acids cannot be synthesized by humans because humans lack the desaturase enzymes required for their production. They form the starting point for the creation of more desaturated fatty acids, most of which also have a longer carbon chain:

ω-3 fatty acids:
eicosapentaenoic acid or EPA (20:5n-3)
docosahexaenoic acid or DHA (22:6n-3)
ω-6 fatty acids:
gamma-linolenic acid or GLA (18:3n-6)
dihomo-gamma-linolenic acid or DGLA (20:3n-6)
arachidonic acid or AA (20:4n-6)Except for GLA, which has a short 18-carbon chain, these fatty acids have more than 18 carbon atoms and are typically classified as LC-PUFA.ω-9 fatty acids are not essential in humans because they can be synthesized from carbohydrates or other fatty acids. Essentiality in human diet
Mammals lack the ability to introduce double bonds in fatty acids beyond carbon 9 and 10, hence the omega-6 linoleic acid (18:2n-6; LA) and the omega-3 Alpha-linolenic acid (18:3n-3; ALA) are essential for humans in the diet. However, humans can convert both LA and ALA to fatty acids with longer carbon chains and a larger number of double bonds, by alternative desaturation and chain elongation. In humans, arachidonic acid (20:4n-6; AA) can be synthesized from LA.