Bridging the Gap between Psychiatry and Neurology: Alzheimer's disease- symptoms beyond memory impairment

Abstract

It is increasingly recognized that there is significant heterogeneity in phenotype and clinical trajectories in Alzheimer's disease.Up to 25% of Alzheimer's disease (AD) cases do not show the typical neuropathology. Recently subtypes and atypical non-amnestic AD presentations have been formalized in the International Working Group (IWG) clinical diagnosis criteria. Clinical diagnosis of atypical AD has significantly been improved by the availability of biomarkers, including cerebrospinal fluid levels of Aβ42, total tau (t-tau) and phosphorylated tau181 (p-tau), MRI volumetric estimation of hippocampal and medial temporal atrophy, and amyloid brain PET imaging. Special attention will be given to language variant of Alzheimer's disease. A predominant deficit in the language domain is a key feature of primary progressive aphasia but language impairment is commonly present in Alzheimer's disease. International diagnostic criteria for PPA and its three variants (agrammatic, logopenic, semantic) were published in 2011. Since then, studies have investigated the validity of these criteria in classifying patients which includes clinical symptoms, neurocognitive presentations, distinct MRI signatures, and neuropathological differences. In this session special attention will be given of logopenic PPA a syndrome frequently seen in atypical Alzheimer's disease. Even though Alzheimer's disease is most notable for memory impairment, language impairments are also found early in the disease course. Indeed, neuropsychological testing shows changes in confrontation naming and semantic fluency. However, there is an additional body of research that shows that changes in spontaneous language, including idea density, speech quantity, fluency, and tempo can differentiate between normal aging and Alzheimer's disease.A physiologic sleep pattern is essential in the process of memory formation. Inadequate sleep results in cognitive impairment. MCI has an increased rate of sleeping problems compared to healthy people of the same age. In MCI, primary sleep disorders like sleep-disordered breathing, PLMS, RLS, RBD are more common, and also associated with a high rate of progression from MCI to AD. MCI also showed shorter total sleep time (longer in non-amnestic MCI), sleep efficiency, and cyclic alternating pattern. There is increased nighttime behavior. EEG power in amnestic MCI showed a reduction in the power of delta and theta frequency. There is a reduction in fast spindle counts on frontal location. Blunted and delayed onset with a duration of REM sleep reduced. A growing body of evidence supports the hypothesis that people with sleep disorders have a higher risk of developing Alzheimer's disease AD. Insomnia, self-reported sleep disturbances, decline in sleep duration, impaired sleep consolidation, delayed or decreased circadian rhythms and sleep-disordered breathing have been shown to increase AD risk, supporting the hypothesis that a chronically disrupted sleep-wake cycle can drive AD pathogenesis. Associations of sleep disorders and neurodegeneration in Alzheimer's are complex. Its understanding however is crucial for proper AD prevention, diagnosis, as well as management.Psychosis is a core syndrome in other than Alzheimer's disease and neurodegenerative disorders. It is however present in a large percentage of patients with AD. Psychosis most commonly presents as a delusional process and is linked to disruptive behavior, rapid progression, and overall morbidity. Psychotic syndromes in AD are complex but necessary to be diagnosed and managed properly.