A Direct Line From Dietary Linoleic Acid To Alzheimer's Disease?

Sure looks like it (PDF).

4-hydroxy-2-noneal (4-HNE) is produced in the mitochondria of those with excess amounts of linoleic acid (LA) in their diets.  It turns out it's also important in Alzheimer's and other neuro-degenerative diseases.

"The mitochondrial enzyme ALDH2 exerts an important physiological protection in a variety of tissues, as it degrades highly toxic aldehydes originating from the lipid peroxidation cascade, mainly 4-HNE. Protection afforded by ALDH2 has been observed in conditions in which oxidative stress and the resulting excessive production of 4-HNE causes tissue damage, often evolving toward degenerative processes (Ohsawa et al., 2008; Wey et al., 2012). Thus, ALDH2 appears to be implicated in diverse pathologies such as Alzheimer’s and Parkinson’s diseases and ischemic conditions (Ohsawa et al., 2008; Wey et al., 2012). Here, we examined the role of ALDH2 in the development of endothelial dysfunction produced by the vasculotropic amyloid Ab (Ab1–40), known to be involved in the pathogenesis of the Alzheimer-associated cerebral amyloid angiopathy (CAA) (Donnini et al., 2010)."

So if they increase ALDH2, they decrease 4-HNE, and reduce the damage to the cell.

"The present work identifies a specific detoxifying mechanism, provided by activation of a mitochondrial enzyme, ALDH2, by means of the selective activator Alda-1. The protection of the vascular endothelium from injuries arising from toxic products of lipid peroxidation [4-HNE] afforded by this activator could have implications for a wide range of diseases in which impairment of mitochondrial function and angiogenesis are the underlying pathogenetic mechanism. Our findings, demonstrating that activation of ALDH2 by Alda-1, prevents the injurious effects of Ab on vascular endothelium and preserves angiogenic phenotype and responsiveness, may have applications for other age-related vasculopathies, including those associated with diabetes and vascular dementia."

Their are other ways to reduce "toxic products of lipid peroxidation", that don't require more research.