Introduction
The amyloid deposition has long been considered one of the pathognomonic markers of Alzheimer’s disease (AD). Moreover, disruption in the amyloid hypothesis has been frequently discussed as an important target of intervention for many years. Early detection of amyloid detection has occurred as a major target of intervention in AD patients. In this regard, amyloid imaging has emerged as an effective diagnostic tool that could enable early intervention in patients in AD trajectory. Amyloid deposition usually initiates from temporal and orbitofrontal cortices, which later extends to frontal, parietal, precuneus, anterior and posterior cingulate cortices.
Case Presentation
A 37-year-old male patient presented with complaints of gradual cognitive decline, apraxia, disorientation, and sleep disturbances.
Physical Examination
- The laboratory findings did not reveal any abnormalities, and the tests for human immunodeficiency virus, syphilis all turned out to be negative.
- A neuropsychological test battery was implemented to evaluate the patient’s cognitive status.
- In the cognitive tests, in contrast to the relatively preserved language function, he displayed serious impairments in free recall, 20-minute delayed recall and recognition.
- Brain magnetic resonance imaging indicated global cerebral atrophy of grade 1 by cortical atrophy scale and notable medial temporal lobe atrophy of grade 2 by medial temporal lobe atrophy visual rating scale.
- Atypically early onset of dementia symptoms made the patient an eligible candidate for amyloid positron emission tomography (PET) imaging.
- 18-Florbetaben PET images revealed diffuse amyloid deposition with score 3 in brain beta-amyloid plaque load (BAPL), with predominant amyloid deposition in the striatum.
Family History
- No family history of similar complaints was found.
Clinical Examination
- The patient indicated early onset of cognitive decline with accelerated deterioration.
- Working as an industrial researcher, the patient started to make serious calculation mistakes that made him quit the job.
- However, his frequent forgetfulness, along with aggravation in recent memory impairments hampered him from fulfilling his duties.
- Apraxia and apathy had started 2 years ago and disorientation to time and person was worsened.
- The patient’s sleep disturbance became prominent, frequently waking up in the middle of the night self-talking.
Treatment
- 5 mg of donepezil was prescribed, and the patient was discharged on the 10th day of his admission.
- To control his persistent cognitive decline even after the discharge, donepezil was increased up to 23 mg with a combination of memantine, which was also increased up to 20 mg.
Clinical Outcome
The cognitive decline has been relatively plateaued but the patient was advised to regularly visit the clinic for monitoring of his symptoms.