Formaldehyde (FA) is a highly reactive carbonyl species recognized for its applications as a tissue fixative and embalming agent due to its potent capacity to cross-link DNA and protein through formation of stable methylene bridges. Exposure to exogenous FA via inhalation or ingestion poses a significantthreattohumanhealth.FAoverload,forinstance,can damage the central nervous system leading to reduced performance in memory and cognitive abilities.1,2 However, the endogenous production of FA is a normal physiological process mediated by enzymatic systems such as semicarbazidesensitive amine oxidase (SSAO) that generate FA and opposing molecular mechanisms that remove it.3 In the brains of healthy individuals,theconcentrationofFAisinthe0.2−0.4mMrange4 andhasbeenproposedtoplayaroleinthestorage,preservation, andretrievaloflong-termmemorythroughDNAdemethylation cycles.5 However, FA is elevated in patients afflicted with neurodegenerative diseases such as Alzheimer’s disease (AD) due to an overexpression of SSAO.6 Indeed, abnormally high levels of FA, 0.5 mM, were found in the brain tissues of AD animal models.7 In this context, FA is neurotoxic and has been shown to degrade neuronal networks through induction of hyperphosphorylation and polymerization of the τ protein.8 Additionally, FA was reported to induce β-amyloid misfolding and aggregation via intramolecular and intermolecular crosslinking between lysine residues (Lys16 and Lys28).9 An assortment of methods including colormetric assays,10 HPLC,11,12 andGC13 analysesfollowingchemicalderivatization,