Alzheimer disease, or Alzheimer’s in the anglo-saxon world, is commoner in Latin American than in developed nations, and the resources in the continent are lacking in comparison. There is almost no official budget, little epidemiological data, and minimal mental health facilities. Diagnosis is often wrong in the wider field of dementia, as few physcians with knowledge exist, and the population is fertile with stigmas ( Mario Parra et al Neurology 2018, 90:222-231).
There are 3 imaging biomarkers established for the diagnosis of Alzheimer disease: hippocampal volumes, as shown in the figures; white matter lesions; and amyloid deposits as viewed on positron- emmission tomography. PET-CT does not help, amyloid is viewed on fluorodeoxyglucose of florbetapir PET scans, and MRI needs to be at least 1,5T to accurately demonstrate abnormalities. These findings – Lopez et al, Neurology 2018, e1920-1928 – were confirmed in a study of 183 patients in Pittsburgh, USA, followed biannually between 2009 and 2017.
Imaging and clinical studies indicate that patients with lesser hippocampal atrophy at onset may be predicted to follow a faster cognitive decline – Risacher et al, Neurology 2017, 89:2176-2186. In other words, patients in the hippocampal sparing group had increased tau mayloid deposition, started the disease earlier, and progressed faster than those with hippocampal or lymbic subtypes. Retrospectively, patients with Minimental tests in the region of 23 could be predicted in this manner. The early clinical marker was in executive function measured by a composite test.
PET scans using florbetapir have been shown to follow in vivo the pattern of tau deposition demonstrated in neuropathological studies of people with Alzheimer disease. Tau amyloid deposits appear in temporobasal and frontomedial areas, progress to the associative neocortex, then primary sensory and motor areas. Then the medial temporal lobe is involved, and finally the striatum. Only 2% of 667 patients progressed differently from this 4-stage model – Grothe et al. Neurology2017, 89-2031-2038
Prof. Paulo Bittencourt, MD, PhD, FAAN
