Background: Vitamin B12 deficiency is widely known for its hematological and neurological manifestations. Neuropsychiatric manifestations of vitamin B12 deficiency include dementia, delirium, cerebellar ataxia, psychosis, neuropathy, and mood disorders. Dementia caused by vitamin B12 deficiency may not be accompanied by anemia and it may be the sole manifestation of cobalamin deficiency. Case description: A 70-year-old woman, premorbid normal, presented with rapidly progressive cognitive impairment over a period of 7 months in the form of short-term and episodic memory disturbances, decreased interaction, withdrawn behavior, apathy, wayfinding difficulties, and sleep disturbances. Neurologic examination revealed a mini-mental state examination (MMSE) score of 9/30. Tests for attention and sustained attention were impaired. Speech and language examination revealed reduced word output and impaired animal naming. Both immediate and recent memory was impaired. Lobar examination revealed frontal and temporal involvement. The patient's initial laboratory investigations indicated mildly decreased hemoglobin (10.2 gm/dL) and normal MCV - 98 fL. There were very low levels of vitamin B12 (116 pg/mL). Magnetic resonance imaging (MRI) of the brain showed age-related cortical atrophy. The patient was treated with parenteral methylcobalamin initially then switched to oral cobalamin. After a period of 3 months of treatment, MMSE was reassessed and was 16/30. She was fully oriented and had significant improvement in her memory and behavior. Conclusion: The role of vitamin B12 deficiency as one of the few treatable causes of dementia, however, is still controversial. The purpose of this case report is to show that if vitamin B12 deficiency remains undiagnosed, serious sequelae may occur. Assessment of B12 levels should be included as a standard evaluation in patients presenting with dementia. Therefore, prevention, early detection, and management of this reversible state are of profound importance.