Abcd2, also known as the adrenoleukodystrophy-related gene, is a potential therapeutic target for X-linked adrenoleukodystrophy. Its up-regulation can compensate for ABCD1 deficiency, restoring peroxisomal β-oxidation of very-long-chain fatty acids. Multiple factors can induce the expression of ABCD2, including phenylbutyrate, histone deacetylase inhibitors, fibrates, dehydroepiandrosterone, thyroid hormone, thyromimetics, LXR antagonists, and 22S-hydroxycholesterol [4].

The ABCD2 score, which is related to the ABCD2 gene, is used in clinical settings to assess stroke risk. However, studies show its limitations. For example, it has low specificity for recurrent stroke within 7 days (35.4%, 95% CI 33.3%-37.6%) and fails to reliably discriminate low-and high-risk patients for early recurrent stroke. Also, it cannot effectively identify patients with carotid stenosis or atrial fibrillation needing urgent intervention, nor streamline clinic workload [2]. In diagnosing stroke in patients with dizziness or acute vestibular syndrome, clinical decision rules like HINTS outperform the ABCD2 score in terms of sensitivity, specificity, and likelihood ratios [1,3,5]. Additionally, in differentiating central from peripheral causes of acute vertigo, the ABCD2 score has a low sensitivity (55%) and fails to predict half of central vertigo cases [3].

In conclusion, the Abcd2 gene is crucial for peroxisomal function and has potential therapeutic implications for X-linked adrenoleukodystrophy. The related ABCD2 score, while intended for stroke risk assessment, has significant limitations in accurately predicting stroke risk and differentiating central from peripheral causes of dizziness-related symptoms in clinical practice.