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The female patient presented at the age of 45 with a one year history of progressive memory impairment which had been first noticed by her family. Complex tasks, such as resuming newspaper articles or private discussions, were severely limited and the patient relied increasingly on notes. She had lost interest in reading, and spontaneous conversation was notably impeded by word finding difficulties and repetitions. Other early features included spatial disorientation and social retreat. In her work as a secretary she reported not only feelings of deficiency but several overstraining situations. The patient had considerable insight into her forgetfulness and found it distressing.

Medical history was normal except for a depressive episode during adolescence after the early death of her father, who died at the age of 56 of AD, confirmed by autopsy. Neither convulsions nor myoclonus were reported. Diagnostic information on age of onset, duration, symptom presentation and progression of the disease were confirmed and supplemented by a family member.

In neuropsychological examination the patient’s estimated intellectual level revealed a premorbid IQ of 115, measured by the Mehrfachwahl-Wortschatz-Intelligenztest (MWT-B), revised by Satzger (2002). Naming (Aachener Aphasie Test), visuoconstructive skills (clock-test and Rey-Osterrieth figure drawing Test) revealed well preserved skills. Semantic verbal fluency, however, was significantly reduced (Regensburger Wortflüssigkeits-Test (###865###RWT)). Speed of cognitive information processing (Zahlen-Verbindungs-Test (ZVT)) was decreased and cognitive flexibility (Trail-Making –Test B (TMT B)) was significantly limited.

At presentation she demonstrated word finding problems and tended to give concrete interpretations to proverbs. Semantic or phonematic paraphasias did not occur. Mini-Mental State Examination score was 25/30; the Consortium to Establish a Registry of Alzheimer’s Disease Neuropsychological Battery (CERAD-NP) (Welsh et al., 1994) showed deficits in Word List Memory and Recall, Word List Recognition, Word List Recall and Recall of Constructional Praxis. However Naming and Constructional Praxis were normal.

At the time of her first assessment in 2004 the patient already had a severe global memory impairment. Verbal and visual memory functions were assessed with the California Verbal Learning Test, the Wechsler Memory Scale Revised (WMS-R) and the Benton test and showed significantly decreased skills in free und cued word list memory, recall and recognition. Verbal und visual working memory skills were substandard. Verbal immediate memory was normal, whereas visual immediate memory was decreased.

General physical and neurological examination was normal. A Hashimoto's thyroiditis was ruled out, even though a routine blood examination disclosed slightly increased TPO antibodies. APOE genotype was determined as e2/3. CSF analysis showed AD-typical measures of increased total tau protein and decreased Aß42, findings for protein 14-3-3 were negative. An eelectroencephalography (EEG) showed abnormal findings with alpha activity and intermittent theta activity. An examination of visual evoked potentials (VEP) showed no pathological findings. A magnetic resonance imaging (MRI) scan revealed marginal cortical, fronto-temporal atrophy. ¹⁸F-fluoro-2-deoxy-glucose scans (¹⁸F-FDG PET) showed moderate metabolic deficits at the left hemisphere including the temporal and parietal lobe, the posterior cingulate region and both of the frontal lobes. The patient had been diagnosed with probable AD and initially been treated with Donezepil.

Upon re-examination in 2006, the patient complained of increasing forgetfulness and word finding problems. Even though sequences of work processes were being prepared the patient experienced increasing difficulties in sustaining attendance at work. She developed frequent episodes of temporal and spatial disorientation and had become dependent in household activities. She scored 24/30 in the MMSE, psychometric testing by CERAD showed mild, progressive deterioration, the clock drawing test disclosed a noticeable impairment in line spacing. Abstract thinking was impaired, revealing massive difficulties in explaining proverbs and forming generalisations. Mood was stabile under antidepressant medication. Mild apraxia was found during neurological examination. An MRI scan at that time showed dilatation of the internal and external CSF spaces, marked cerebral atrophy and mild white matter lesions. A follow-up ¹⁸FDG PET exhibited a marked parieto-temporal hypometabolism more apparent on the left. The preliminary exam showed solely a left parietal hypometabolism. The decreased rate of metabolism in the left temporal, both frontal and cingulate region progressed.

Further decline was evident in the following year. The patient suffered from further loss of memory, concentration and aphasia and finally had to retire from work. Spatial disorientation increased, the patient had become entirely dependent on external help and required full time supervision. A weight gain of 5 kg resulted from increased appetite and an apathetic state. The patient had to be admitted to a specialized memory day clinic due to mood instability and anxiousness besides the symptoms of cognitive decline and was treated with Galantamine and Memantine.