Today, I link to a Google search Scholarly articles for scholarly articles on neuroradiologic evaluation in patients with subjective cognitive decline. Accessed 10-7-2-24.
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- Subjective Cognitive Decline and Related Cognitive Deficits. [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Front Neurol. 2020; 11: 247.
Published online 2020 May 19. doi: 10.3389/fneur.2020.00247
- Subjective cognitive decline: opposite links to neurodegeneration across the Alzheimer’s continuum. [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Brain Commun. 2021; 3(3): fcab199. Published online 2021 Sep 1. doi: 10.1093/braincomms/fcab199
- Recent contributions to the field of subjective cognitive decline in aging: A literature review. [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Alzheimers Dement (Amst). 2023 Oct 18;15(4):e12475. doi: 10.1002/dad2.12475. eCollection 2023 Oct-Dec.
- “There is mixed evidence supporting nutritional interventions in SCD, although stronger evidence for improved cognition and increased brain activity in individuals with SCD was seen in studies using shentai tea polyphenols, fermented dairy products (e.g., β‐lactolin found in products such as yogurt), and combinations of nutrients, with less promising evidence for beneficial effects using other supplements such as vitamin D, specific proteins, and amino acids. 139 , 140 , 141 , 142 “
- SCD has been and continues to be linked to both structural and functional neuroimaging correlates. Compared to healthy controls, individuals with SCD show differences in both gray and white matter structure, 64 including reduced hippocampal and basal forebrain volume and cortical thinning in frontal, temporal regions, 65 , 66 , 67 , 68 , 69 as well as both local 70 and widespread differences in white matter. 65 , 71 , 72 These differences are related to subtle cognitive deficits in SCD. 46 , 68 , 69 , 73 , 74 Recent studies have also highlighted the heterogeneous relationship between brain structure and SCD, which may be influenced by factors such as the study setting (i.e., clinical vs community). 64 , 75 The disease stage may also be a key moderator; at early stages, greater levels of SCC were associated with lower gray matter volume and reduced glucose metabolism, whereas at later stages of the AD continuum when cognition is impaired and insight is lessened, lower levels of SCC were related to greater neurodegeneration. 75 “
- Structural neuroimaging changes associated with subjective cognitive decline from a clinical sample. [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Neuroimage Clin. 2024:42:103615. doi: 10.1016/j.nicl.2024.103615. Epub 2024 May 10.
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- “Abstract
Background
Alzheimer’s disease (AD) is characterized by progressive deterioration of cognitive functions. Some individuals with subjective cognitive decline (SCD) are in the early phase of the disease and subsequently progress through the AD continuum. Although neuroimaging biomarkers could be used for the accurate and early diagnosis of preclinical AD, the findings in SCD samples have been heterogeneous. This study established the morphological differences in brain magnetic resonance imaging (MRI) findings between individuals with SCD and those without cognitive impairment based on a clinical sample of patients defined according to SCD-Initiative recommendations. Moreover, we investigated baseline structural changes in the brains of participants who remained stable or progressed to mild cognitive impairment or dementia.” - ”
1. Introduction
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive deterioration of cognitive function, leading to the loss of functional independence. It is also the most frequent cause of dementia in older adults (Scheltens et al., 2016). Studies have found that some individuals with subjective memory complaints exhibit clinical progression to mild cognitive impairment (MCI) or dementia due to AD (Jessen et al., 2014, Molinuevo et al., 2017, Rabin et al., 2017). According to the National Institute on Aging–Alzheimer’s Association criteria, subjective cognitive decline (SCD) can be considered as stage 2 within the AD continuum (Jack et al., 2018). Considering the lack of standardized criteria for defining SCD, in 2014, the SCD-Initiative working group (SCD-I) proposed a conceptual framework and a set of terminologies and features for SCD relying on two main criteria: (1) self-experienced persistent decline in previously normal cognitive capacity unrelated to an acute event and (2) normal performance on standardized cognitive tests, which are used to classify MCI, adjusted for age, sex, and education. Additionally, this decline cannot be explained by a psychiatric or neurological disease (apart from AD), medical disorder, medication, or substance use (Jessen et al., 2014, Molinuevo et al., 2017). Although the SCD-I criteria have been recommended for research contexts, other methods are currently being used (Morrison et al., 2022;33:102923.).” - “The present study aimed to establish the morphological differences associated with SCD on brain MRI at diagnosis and their association with clinical progression in a clinical sample of patients defined according to SCD-I recommendations. Precisely, we examined baseline volumetric differences in GM and WM between patients with SCD and HCs. We also compared baseline GM and WM volumes between HCs and those with SCD who exhibited clinical progression (SCDp) or remained cognitively stable (SCDnp) at follow-up. GM volume was assessed using two common techniques for brain volumetric analyses, namely VBM and ROI. We further determined the WML burden in each group.”
- “All patients with SCD (n = 309; age, 65.4 ± 9.4 years) satisfied the research criteria proposed by SCD-I. They complained of memory decline despite having a normal performance on standardized neuropsychological tests. Among the 309 participants, 99 who completed one or more follow-up visits up to January 2020 after baseline were analyzed through a retrospective longitudinal follow-up at our unit. During the follow-up visits, the patients were evaluated by a neurologist, and a neuropsychological assessment was performed to assess clinical progression, which included the same neuropsychological evaluation criteria as the initial evaluation. Notably, 32 participants progressed to amnestic MCI (n = 24) or dementia (n = 8), based on the 2011 NIA-AA clinical criteria (Albert et al., 2011, McKhann et al., 2011), and were classified as SCD progressors (SCDp; n = 32; age, 71.0 ± 5.8 years). Interestingly, none of the patients with SCD who exhibited progression had another type of dementia other than AD based solely on clinical diagnostic criteria without assessing for AD biomarkers of amyloid or tau deposition.”
- “All participants underwent the following initial assessment: (1) medical and history review, (2) interview with a family member or friend, (3) general examination, and (4) neurological examination and a neuropsychological assessment. The medical history and variables included age at SCD diagnosis, sex, education level, and history of medical conditions such as hypertension, diabetes mellitus, hypercholesterolemia, smoking habit, and cardiovascular or cerebrovascular disease. General medical examination included a laboratory test (full blood count, biochemistry, vitamin B12, serum folate, glucose, lipids, syphilis serology, and thyroid function) and brain MRI (1.5-T MRI; T1- and T2-weighted 2D FLAIR). The standardized cognitive tests to evaluate cognitive status at baseline and follow-up included a comprehensive test battery that evaluated the following domains: global cognitive function (Mini-Mental State Examination [MMSE]) (Folstein et al., 1975); episodic verbal memory (word list learning, recall, and recognition), and episodic visual memory (figure recall) (The Consortium to Establish a Registry for Alzheimer’s Disease Word List Memory Task [CERAD] neuropsychological battery) (Morris et al., 1988); attention and executive function (Trail Making Test parts A and B) (Reitan and Wolfson, 1993); phonetic fluency (words with letter p) (Ramier and Hecaen, 1970); cognitive flexibility and cognitive interference (The Stroop Color and Word Test) (Golden, 1978); semantic fluency (animal categories) (Ramier and Hecaen, 1970); and the 60-item Boston naming test (Kaplan et al., 2001). Depression and activities of daily living function were evaluated using the 30-question Geriatric Depression Scale (GDS) (Yesavage et al., 1982) and Interview for Deterioration in Daily Living Activities in Dementia (IDDD) (Teunisse et al., 1991), respectively. Normal cognition was operationalized by a performance exceeding − 1.5 standard deviations (SD) from the normal range adjusted for age, sex, and education on all tests (Molinuevo et al., 2017).”
- “The exclusion criteria for patients were as follows: (1) age less than 56 years, (2) MCI or dementia, (3) major neurological disorders or systemic illnesses that could cause cognitive impairment, (4) current or past major psychiatric disease, such as schizophrenia, major depression, or bipolar disorder), (5) history of alcohol or substance abuse, (6) significant brain MRI abnormalities, such as brain tumors, large cerebral infarct, or bleeding, and (7) history of head trauma with loss of consciousness. Unimpaired cognitive performance in the HC group was defined using the same definition as the SCD group. All records were reviewed in a multidisciplinary consensus meeting to establish a clinical diagnosis.”
- 2.2. MRI acquisition and processing: See text for details.
- “Although this study was performed using a large memory center sample of patients with SCD, the number of samples evaluated to determine clinical progression in the subgroups was small. Additionally, four types of studies were performed on the same sample, including 120 ROIs during analysis. Nevertheless, some limitations of our study must be noted. First, the current research was a retrospective database analysis, which precluded a more homogeneous sample selection or the performance of a prospective longitudinal follow-up on the total SCD sample owing to data unavailability. Second, patients were scanned using two different 1.5-T MRI scanners under different parameters, which may have affected our results. However, sex, age, education level, scanner type, and total intracranial volume were included as covariates during analyses. Third, the HC group was smaller in size than the SCD group and had different medical and demographic conditions, which may have caused bias due to the lack of knowledge regarding factors present as biomarkers of amyloidosis, tau burden, or APOEε4 carriers (Rabin et al., 2017). Fourth, patients whose disease progressed to another stage of cognitive impairment did not undergo brain MRI during follow-up, although a neuropsychological follow-up was performed. Therefore, the longitudinal follow-up was only used to determine clinical progression and not changes in MRI findings. Fifth, although WM tract analysis was performed using VBM, diffusion MRI analysis was not performed despite the similar findings. Sixth, although T2-weighted 2D FLAIR sequences were used to quantify WML, 3D FLAIR sequences could facilitate the detection of small WML (Paniagua Bravo et al., 2014).”
- “In conclusion, participants with SCD exhibited reduced GM volume in the frontal lobe, occipital lobe, precunei, and thalami. MTL (medial temporal lobe) atrophy was observed on baseline MRI among patients with SCD who experienced clinical disease progression. These findings support the initial heterogeneity of the syndrome and reinforce previous knowledge suggesting that structural damage in the hippocampus and amygdalae would have already begun during the long presymptomatic period of AD. Moreover, the affected GM regions in the cerebral cortex were anatomically correlated with the impaired WM tracts in patients with SCD. Although numerous studies have reported a relationship between WML and cognitive decline, no significant differences were observed in our sample. Hence, future longitudinal studies with larger samples of patients with SCD-plus, which includes more features probably observed in preclinical AD, are needed to assess the cognitive trajectory of subjects who exhibit cognitive impairment progression.”
