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Neuropsychiatric Disturbances in Alzheimer's Disease: What Have We Learned from Neuropathological Studies?

Van Dam, D., Vermeiren, Y., Dekker, A. D., Naude, P. J. W. & De Deyn, P. P., 2016, In : Current alzheimer research. 13, 10, p. 1145-1164 20 p., 13.

Research output: Contribution to journalReview articleAcademicpeer-review

Neuropsychiatric symptoms (NPS) are an integral part of the dementia syndrome and were therefore recently included in the core diagnostic criteria of dementia. The near universal prevalence of NPS in Alzheimer's disease (AD), combined with their disabling effects on patients and caregivers, is contrasted by the fact that few effective and safe treatments exist, which is in part to be attributed to our incomplete understanding of the neurobiology of NPS. In this review, we describe the pathological alterations typical for AD, including spreading and evolution of burden, effect on the molecular and cellular integrity, functional consequences and atrophy of NPS-relevant brain regions and circuits in correlation with specific NPS assessments. It is thereby clearly established that NPS are fundamental expressions of the underlying neurodegenerative brain disease and not simply reflect the patients' secondary response to their illness. Neuropathological studies, moreover, include a majority of end-stage patient samples, which may not correctly represent the pathophysiological environment responsible for particular NPS that may already be present in an early stage, or even prior to AD diagnosis. The burdensome nature and high prevalence of NPS, in combination with the absence of effective and safe pharmacotherapies, provide a strong incentive to continue neuropathological and neurochemical, as well as imaging and other relevant approaches to further improve our apprehension of the neurobiology of NPS.

Original languageEnglish
Article number13
Pages (from-to)1145-1164
Number of pages20
JournalCurrent alzheimer research
Volume13
Issue number10
Publication statusPublished - 2016

    Keywords

  • Aggression, amyloid, depression, neurofibrillary tangles, neuronal loss, psychosis, neurotransmitter, MILD COGNITIVE IMPAIRMENT, LEWY BODY VARIANT, LATE-LIFE DEPRESSION, GELATINASE-ASSOCIATED LIPOCALIN, NEUROFIBRILLARY TANGLE DENSITY, UBIQUITIN PROTEASOME SYSTEM, PARAMETRIC MAPPING ANALYSIS, AMYLOID-BETA PEPTIDES, DEFAULT MODE NETWORK, A-BETA

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