A 44-year-old previously healthy man with a 9-month history of progressive cognitive decline, depression, urinary incontinence, and inability to perform tasks of daily living presented to the emergency department with worsening cognitive and neuropsychiatric symptoms. He had become more distressed, and his family noticed him departing the house without closing doors, leaving water faucets running, and sending his children to school on Sundays. History taken from the patient’s wife revealed that his brother had passed away in his late 30s after a slowly progressing functional and cognitive decline over the course of 5 years. No further detailed family history could be obtained. The review of systems was negative; he had no prior medical, psychiatric, or surgical history; and he denied any history of recent travel, camping, hiking, or vaccination. The patient was not taking any dietary supplements, nor was he taking any over-thecounter or prescription medication. Examination revealed vital signs were within normal limits. Neurocognitive assessment revealed a conscious, coherent, and alert patient with impaired memory and concentration. He showed poor attention, depressed mood, and restricted affect. He was unable to spell the word world forward, nor was he able to understand a request to spell it backward. The rest of the physical and neurologic examination revealed no abnormalities. Extensive laboratory work-up was conducted and included the following: toxicology screening; screening for HIV-1, HIV-2, and syphilis treponemal antibodies; COVID-19 polymerase chain reaction; and measurement of B1 and B12 levels. The results of screening were negative. Cerebrospinal fluid (CSF) assays, including CSF oligoclonal bands and CSF flow cytometry, revealed values within normal limits. CT of the brain without intravenous contrast material was performed in the emergency department to rule out acute intracranial abnormality (Fig 1). Multiplanar multisequence MRI of the brain without and with intravenous contrast material was ordered for further assessment (Figs 2–4). CT images of chest, abdomen, and pelvis were unremarkable (images not shown).CT of the brain without intravenous contrast material showed punctuate calcific foci with a stepping-stone appearance in the subcortical and periventricular white matter, best appreciated on sagittal reformatted images (Fig 1). MRI of the brain showed confluent white matter hyperintensities on fluid-attenuated inversion recovery images with frontal predilection that spared subcortical U fibers and involved the corpus callosum (Fig 2). Diffusion-weighted imaging revealed multiple small hyperintense lesions along the deep white matter (Fig 3) without associated contrast enhancement on T1-weighted contrast-enhanced MRI scans (Fig 4A). Brain atrophy was more pronounced in the frontal lobes and was associated with diffuse thinning of the corpus callosum (Fig 4B). On the basis of the imaging findings, a diagnosis of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia was suggested. Later, the patient underwent genetic testing, which revealed a heterozygous mutation of the gene colony-stimulating factor 1 receptor (CSF1R) and served to confirm the diagnosis. What is your diagnosis?