Resting-state synchrony between the retrosplenial cortex and anterior medial cortical structures relates to memory complaints in subjective cognitive impairment

Functional neuroimaging in subjective cognitive decline: current status and a research path forward

“…Lower functional connectivity between default mode and medial temporal structures in SCD [18,37,38,41,47] could either reflect cohort differences compared to analyses noting greater functional connectivity in SCD [30,31,35,36] or represent a later phase of SCD close to mild cognitive impairment conversion marked by decreased signaling capability between regions. While involved in episodic memory, cortical midline regions of the default mode network also mediate self-referential processing [69,88].…”

“…The confounding variables responsible for discrepancies in the results remain unclear; however, a few differences across samples could help explain the results. For example, [18] found lower fractional anisotropy in the superior longitudinal fasciculus and higher fractional anisotropy in the parahippocampal cingulum in individuals with SCD that significantly associated with the functional connectivity of cortical midline structures. Aberrant diffusion characteristics involving physical connections between memory and self-referential regions may distinguish this sample from the others and may reflect a mechanism for lower functional connectivity unrelated to mechanisms underlying increased connectivity [30,31,35].…”

“…Some groups have reported greater connectivity, mainly within and between default mode network and medial temporal regions, in older adults with SCD [30,31,35,36]. However, many groups have also observed lower connectivity between these regions in individuals with SCD [18,[76][77][78][79]. Others have reported no difference from control [60], or intricate patterns of greater and lower functional connectivity in individuals with SCD [51][52][53][54][55], suggesting that a complex reorganization of processing responsibilities across network nodes may occur.…”

“…The extant literature suggests that recruitment methods may indeed contribute to SCD sample characteristics, with cohorts recruited from memory clinics exhibiting poorer neuropsychological performance, greater hippocampal atrophy, greater cortical atrophy over time, and greater depression than cohorts recruited from the general population that have not sought medical help [93][94][95]. However, as samples that have sought medical help have exhibited both increased and decreased functional connectivity cross-sectionally [18,30,47], the impact of the severity of cognitive complaint on functional metrics is not as clear. Future research should aim to further clarify if recruitment methodology is an important predictor of the type of functional connectivity pattern exhibited in SCD.…”

“…According to the modern research definition by the National Institute on Aging and the Alzheimer's Association [10], Alzheimer's disease is a designation for individuals who exhibit pathological amyloid-β and tau deposits, determined either through positron emission tomography or cerebrospinal fluid evaluation. Although discussion of SCD biases towards a precursor to AD, and SCD associates with future dementia development [1,3], associations between SCD and amyloid-β and tau burden are mixed [11][12][13][14][15][16][17][18]; thus, an Alzheimer's-centric approach could misguide interpretation of SCD data. Although AD may be the most common dementia etiology [19], and individuals with SCD may receive an AD diagnosis over time, SCD possibly serves more accurately as a branching point between cognitively intact aging and a myriad of potential outcomes, including various dementias but also, commonly, recovery to a subjectively unimpaired state.…”