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Neurodegeneration is often measured by longitudinal brain atrophy on structural magnetic resonance imaging, indicating a cumulative decrease
Figure 1: Cover art of the paper
Recent work has highlighted the important role of synaptic degeneration and dysfunction by quantifying proteins that reflect presynaptic vesicle mechanisms (synaptosome-associated protein-25 [SNAP-25] and synaptic marker-1[SYT-1]), postsynaptic calcium-mediated signaling pathway regulation (neurogranulins), and extraaxonal growth regulation (growth-associated protein 43 [GAP-43]
CSF NfL and synaptic proteins are increasingly being incorporated into biomarker models of brain aging and Alzheimer's disease (AD) to improve prognosis
The harmful effects of CSF AD protein abnormalities on the medial temporal lobe and total gray matter volume were detected only in people with high (more abnormal) levels of CSF synaptoprotein, even in clinically normal adults
In a cohort of adults without cognitive impairment, Rowan Salner et al.
Core hypothesis: The decrease in gray matter volume associated with NfL is attenuated at lower synaptic dysfunction levels, even taking into account AD pathology (CSF ptau181/Ab42 ratio).
Clinically normal older adults participated in the Hillblom Aging Network Observation Study at the UCSF Center for Memory and Aging and completed baseline lumbar puncture and longitudinal brain MRI (mean scan [follow-up] = 2.
46 clinically normal elderly people (mean age = 70 years; 43% are women) were included
Figure 2: Graph of the paper results
A higher baseline NfL, but not the ptau181/Aβ42 ratio, predicts steeper temporal-crest atrophy (NfL x time: b=-0.
At high NfL concentrations, the atrophy trajectories of low synaptic protein concentrations (b range: -0.
The significance of this study is to find that the link between baseline CSF NfL and longitudinal temporopronic atrophy is accelerated by synaptic dysfunction and buffered
Saloner R, Fonseca C, Paolillo EW, et al.
