Abstract
ABSTRACTBackground: Mild cognitive impairment is considered as the first clinical manifestation of Alzheimer's disease (AD), when the individual exhibits below performance on standardized neuropsychological tests. However, some subjects before having a lower performance on cognitive assessments already have a subjective memory complaint. Objective: A review about subjective cognitive decline, the association with AD biomarkers and risk of conversion to dementia. Methods: We performed a comprehensive non-systematic review on PubMed. The keywords used in the search were terms related to subjective cognitive decline. Results: Subjective cognitive decline is characterized by self-experience of deterioration in cognitive performance not detected objectively through formal neuropsychological testing. However, various terms and definitions have been used in the literature and the lack of a widely accepted concept hampers comparison of studies. Epidemiological data have shown that individuals with subjective cognitive decline are at increased risk of progression to AD dementia. In addition, there is evidence that this group has a higher prevalence of positive biomarkers for amyloidosis and neurodegeneration. However, Alzheimer's disease is not the only cause of subjective cognitive decline and various other conditions can be associated with subjective memory complaints, such as psychiatric disorders or normal aging. The features suggestive of a neurodegenerative disorder are: onset of decline within the last five years, age at onset above 60 years, associated concerns about decline and confirmation by an informant. Conclusion: These findings support the idea that subjective cognitive complaints may be an early clinical marker that precedes mild cognitive impairment due to Alzheimer's disease.
Highlights
The development of disease-modifying treatments for Alzheimer’s disease (AD) targets stages of the disease prior to the dementia syndrome, in which neuronal damage is already irreversible
From the development of biomarkers that allow the detection of β-amyloid peptide, tau protein and neuronal injury, it is known that the AD pathology precedes the onset of dementia by many years.[1,2]
According to the National Institute on Aging-Alzheimer’s Association (NIA-AA), the preclinical phase begins with the cerebral amyloidosis stage, followed by amyloidosis with neurodegeneration, and the subtle cognitive decline stage associated with positive AD biomarkers.[1]
Summary
The development of disease-modifying treatments for Alzheimer’s disease (AD) targets stages of the disease prior to the dementia syndrome, in which neuronal damage is already irreversible. The working group of the National Institute on Aging-Alzheimer’s Association (NIA-AA) has produced new recommendations for the diagnosis of dementia due to Alzheimer’s disease and proposed the concept of AD stages based on the model of the “amyloid cascade”.2. According to this model, the disease runs in a continuous course from the preclinical phase (defined as absence of cognitive decline and presence of positive AD biomarkers) to the mild cognitive impairment stage (decline in at least one cognitive or behavioral domain without functional impairment and the presence of positive biomarker) through to the dementia phase due to Alzheimer’s disease (impairment in at least two cognitive domains with functional decline).[1,3,4] according to the NIA-AA, the preclinical phase begins with the cerebral amyloidosis stage (deposition of β-amyloid), followed by amyloidosis with neurodegeneration, and the subtle cognitive decline stage associated with positive AD biomarkers.[1].
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