The accredited CME learning activity based on this article is offered under the auspices of the CE department of the University of Toronto. Participating physicians are entitled to one (1) MAINPRO-M1 credit by completing this program, found online at www.geriatricsandaging.ca/cme
Progress in basic neuroscience has brought disparate clinical phenotypes of dementia together in categories based on common pathophysiological processes. Degenerative dementias are all proteinopathies featuring abnormal processing and CNS accumulation of different proteins in different neuroanatomic distributions dictating patterns of presentation of clinical symptoms and potential responsiveness to treatment. Alzheimer’s disease (AD) is an amyloidopathy. Dementia with Lewy bodies (DLB), Parkinson’s disease (PD) and multiple system atrophy (MSA) are synucleinopathies. Frontotemporal lobar degeneration (FTLD), progressive supranuclear palsy, and corticobasal degeneration are tauopathies. Vascular dementia (VaD) has been considered a distinct pathophysiologic process yet may exist on a continuum with AD. Currently available dementia treatments are not specific for a single disorder, yet not all dementias are treatment responsive. Exclusion of otherwise treatable depressive disorders and metabolic derangements as well as surveillance for deleterious cognitive effects of medication remain central to the assessment and treatment of the older adult with cognitive complaints. Identification of those syndromes for which certain medications may be contraindicated, as well as those that may be selectively responsive to particular compounds, will continue to increase in importance as our range of therapeutic options widens over the coming years.
Key Words: Alzheimer’s disease, Lewy body, frontotemporal lobar degeneration, vascular dementia, differential diagnosis.