Evolving Evidence for the Value of Neuroimaging Methods and Biological Markers in Subjects Categorized with Subjective Cognitive Decline
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There is evolving evidence that individuals categorized with subjective cognitive decline (SCD) are potentially at higher risk for developing objective and progressive cognitive impairment compared to cognitively healthy individuals without apparent subjective complaints. Interestingly, SCD, during advancing preclinical Alzheimer's disease (AD), may denote very early, subtle cognitive decline that cannot be identified using established standardized tests of cognitive performance. The substantial heterogeneity of existing SCD-related research data has led the Subjective Cognitive Decline Initiative (SCD-I) to accomplish an international consensus on the definition of a conceptual research framework on SCD in preclinical AD. In the area of biological markers, the cerebrospinal fluid signature of AD has been reported to be more prevalent in subjects with SCD compared to healthy controls; moreover, there is a pronounced atrophy, as demonstrated by magnetic resonance imaging, and an increased hypometabolism, as revealed by positron emission tomography, in characteristic brain regions affected by AD. In addition, SCD individuals carrying an apolipoprotein ɛ4 allele are more likely to display AD-phenotypic alterations. The urgent requirement to detect and diagnose AD as early as possible has led to the critical examination of the diagnostic power of biological markers, neurophysiology, and neuroimaging methods for AD-related risk and clinical progression in individuals defined with SCD. Observational studies on the predictive value of SCD for developing AD may potentially be of practical value, and an evidence-based, validated, qualified, and fully operationalized concept may inform clinical diagnostic practice and guide earlier designs in future therapy trials.
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Symptoms of SCD are associated with specific and distinctive underlying pathological events, such as abnormal deposition of ß-amyloid and tau proteins, gray matter atrophy, disruptions in WM and deficits in brain function.
“An increasing number of neuroimaging studies have indicated that the symptoms of SCD are associated with specific and distinctive underlying pathological events, such as the abnormal deposition of ß-amyloid and tau proteins, gray matter atrophy, disruptions in the white matter (WM) and deficits in brain function [3, 10, 11].”
From Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer's disease (2020) · cites this paper as [11]
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“, patients who perform normally on standardized memory tests, but nevertheless report subjective memory impairment) have generally higher levels of Aβ deposition on positron emission tomography (PET) scanning [10, 11].”
BackgroundThe Alzheimer Precision Medicine Initiative
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- Authors
- Lista, S., Molinuevo, J. L., Cavedo, E., Rami, L., Amouyel, P., Teipel, S. J., Garaci, F., Toschi, N., Habert, M.-O., Blennow, K., Zetterberg, H., O’Bryant, S. E., Johnson, L., Galluzzi, S., Bokde, A. L. W., Broich, K., Herholz, K., Bakardjian, H., Dubois, B., Jessen, F., Carrillo, M. C., Aisen, P. S., & Hampel, H.
- Affiliations
- Pitié-Salpêtrière Hospital (FR)
- Alzheimers Disease and Other Cognitive Disorders Unit, Neurology Service, Hospital Clinic, Barcelona, Spain
- Centro San Giovanni di Dio Fatebenefratelli (IT)
- Hospital Clínic de Barcelona (ES)
- Inserm (FR)
- German Center for Neurodegenerative Diseases (DE)
- University of Rome Tor Vergata (IT)
- Centre National de la Recherche Scientifique (FR)
- Royal Swedish Academy of Sciences (SE)
- UCL Queen Square Institute of Neurology (GB)
- University of North Texas Health Science Center (US)
- Trinity College Dublin (IE)
- Federal Institute for Drugs and Medical Devices (DE)
- University of Manchester (GB)
- University of Cologne (DE)
- Medical & Scientific Relations, Alzheimer’s Association, Chicago, IL, USA
- University of California San Diego (US)
- Corresponding author
- Lista, Simone
- ORCID
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2015-09-24
- Volume
- 48
- Issue
- s1
- Pages
- S171-S191
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2173891858
- Cited by
- 53
- References
- 183
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 7 · 2017: 7 · 2016: 4 · 2015: 3 · 2013: 1
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- DZNE Pub (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- subjective cognitive decline, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Cognition Disorders, Humans, Magnetic Resonance Imaging, Neuropsychological Tests, Psychiatric Status Rating Scales, Biomarkers, Disease Progression, Positron-Emission Tomography, Neuroimaging
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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