A 58-year-old male vegetarian presented with progressive numbness and weakness in the lower extremities. Laboratory examinations showed reduced vitamin B12 level with megaloblastic anaemia. Spinal magnetic resonance imaging (MRI) revealed hyperintensity within the posterior and lateral columns on T2-weighted imaging. The diagnosis of subacute combined degeneration (SCD) of the spinal cord was established. Unexpectedly, the patient developed transitory syncope on the second day after hospitalization. The diagnostic computed tomography pulmonary angiography (CTPA) confirmed multiple small pulmonary emboli. An isolated significantly elevated level of homocysteine (117.1 µmol/l) was documented when screening for hypercoagulable markers. Except for a long-term vegetarian diet, no other risk factors for hyperhomocysteinaemia (such as a family history of homocysteinuria) was found. The severity of the hyperhomocysteinaemia found in this current patient was unusual for patients with an insufficient intake of vitamin B12. In SCD patients, elevated homocysteine may increase the risk of thrombosis, which may exacerbate existing problems. Knowing the risk factors should help physicians choose appropriate diagnostic and therapeutic strategies.

Amyotrophic lateral sclerosis (ALS) is biologically heterogeneous, and oxidative injury can contribute to degeneration while also reflecting downstream damage or adaptive responses. Glutathione S-transferase Pi 1 (GSTP1) combines glutathione-dependent detoxification with non-canonical regulation of c-Jun N-terminal kinase (JNK), but the biochemical evidence for direct GSTP1–JNK coupling largely comes from non-ALS systems. This narrative review separates human ALS observations, functional ALS-model findings, and extrapolated mechanisms. Altered GSTP1 abundance or total GST activity in ALS does not establish GSTP1-specific impairment or causality. JNK-related injury has stronger functional support in selected ALS models involving DLK/MAP3K12, ASK1, HIPK2, and MAP4K4. Ferroptosis-related findings are concentrated in SOD1 models, with additional evidence of susceptibility in FUS cellular models, and do not establish a GSTP1–JNK–ferroptosis cascade. We distinguish neuronal and glial context and the execution of apoptosis versus ferroptosis. Decisive tests combine GSTP1 perturbation with catalytic and interaction-deficient rescue, direct binding and JNK-activity assays, and pathway-specific cell-death rescue. GSTP1 remains a candidate context-dependent modifier of shared neurodegenerative processes; causal validation, reproducible pathway biomarkers, and safety assessment are required before therapeutic translation.