A 71 year-old female with thyroid disease presented for rapidly progressive cognitive dysfunction. Three years prior, the patient began to experience difficulty with performing motor tasks and neglecting the right side of her body. Attention and concentration also declined. Gait slowed with shortening of stride length. Memory and ability to name objects remained intact. She had no hallucinations, gaze limitation, dream enactment behavior or myoclonus. She had been placed on donepezil and paroxetine with no improvement. Neurologic examination revealed frontal release signs, ideomotor apraxia and hypomimia. Intermittent dystonia, rigidity and astereognosis of the right hand were seen. Gait examination revealed retropulsion and a slowed gait. Initial testing was within normal limits, including a basic metabolic panel, complete blood count, vitamin B12, thyroid stimulating hormone, Venereal Disease Research Laboratory test, C-reactive protein and erythrocyte sedimentation rate. Cerebrospinal fluid (CSF) testing revealed one red blood cell/uL, one white blood cell/uL, protein of 29 mg/dL, glucose of 54. CSF culture, gram stain and 14-3-3 protein were both negative. Further CSF analysis revealed A-beta 42 (734.75 pg/ml), phospho-tau (70.55 pg/ml) and total-tau levels (453.95 pg/ml) with A-beta 42/total-tau index (ATI; 0.95), borderline for Alzhemier's disease (Values for Alzheimer's: phospho-tau >68 pg/ml; ATI >1.2). Magnetic resonance imaging (MRI) of the brain showed atrophy of the left parietal lobe (Fig. 1). Positive emission tomography (PET) demonstrated reduced uptake in the left parietal lobe (Fig. 2).