Cognitive Assessment Summary

Laboratory assay overview

This panel combines tests to evaluate potential sources of cognitive impairment other than neurodegenerative disease, including markers of kidney, liver, thyroid, and metabolic function (including vitamin B12 metabolism), as well as infections and inflammation. Clinical presentation of cognitive impairment can include alterations in behavior, memory, attention, and planning, including the ability to complete daily tasks, and causes of cognitive impairment can include or be independent of neurodegeneration. Patients with conditions, such as altered mental status, delirium, amnesia, or other acute encephalopathies may experience cognitive impairment from etiologies including metabolic dysfunction, infections, thyroid and hormonal imbalances, pharmacologic interactions, environmental toxins, autoimmune disorders, and other systemic conditions. [1-4] Multiple etiologies for cognitive impairment (e.g., vitamin B12 deficiency, high homocysteine and methylmalonic acid, insulin resistance, poor diet, poor sleep, lack of exercise, chronic inflammation, kidney or liver dysfunction) can present similarly and may co-exist simultaneously. Many of these underlying contributors to cognitive impairment and neurodegeneration are often modifiable, which can improve patient outcomes to prevent or delay disease progression and related complications. [5-7] The Cognitive Assessment Panel with Reflex to FT4 combines various guideline-recommended testing to evaluate other non-neurodegenerative causes of cognitive impairment. [8] Additional tests, such as methylmalonic acid and a reflex to Free T4 are included to provide additional insight to vitamin B12 status and thyroid health, respectively [9,10]. In general, identifying modifiable sources of cognitive impairment can assist providers in differentiating etiologies and improving patient outcomes. The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings. References: 1. Veauthier B, et al. Am Fam Physician. 2021;104(5):461-470. PMID: 34783500 2. Sealy D, et al. Am Fam Physician. 2022;105(1):50-54. PMID: 35029951 3. Todd OM, et al. Clinical Medicine. 2016;16(Suppl 6):s98. doi:10.7861/clinmedicine.16-6s-s98 4. Reddy P, et al. Cureus. 2022;14(2):e22102. doi:10.7759/cureus.22102 5. Attea P, Johns H. J Am Geriatr Soc. 2010;58(8):1587-1590. doi:10.1111/j.1532-5415.2010.02963.x 6. Livingston G, et al. Lancet. 2017;390(10113):2673-2734. doi:10.1016/s0140-6736(17)31363-6 7. Ngandu T, et al. Lancet. 2015;385(9984):2255-2263. doi:10.1016/s0140-6736(15)60461-5 8. Atri A, et al. Alzheimer's Dement. 2025;21(6):e14333. doi:10.1002/alz.14333 9. Wang C, et al. Front Neurol. 2025;16. doi:10.3389/fneur.2025.1594103 10. Alsauskė SV, et al. Medicina. 2024;60(12):1917. doi:10.3390/medicina60121917