Abstract
IntroductionPhysical exercise has gained increasing focus as a potential mean to maintain cognitive function in patients with Alzheimer's disease (AD). Alongside the markers of specific AD pathology (amyloid β and tau), other pathologies such as neuronal damage and synaptic loss have been proposed as markers of the disease. Here, we study the effect of physical exercise on biomarkers of neuronal and synaptic integrity. MethodsCerebrospinal fluid (CSF) from 51 AD subjects who participated in the randomized controlled trial Preserving Cognition, Quality of Life, Physical Health and Functional Ability in Alzheimer's Disease: The Effect of Physical Exercise (ADEX) was analyzed for the concentration of neurofilament light (NFL), neurogranin (Ng), visinin-like protein-1 (VILIP-1), and chitinase-3–like protein 1 (YKL-40). Participants were subjected to either 16 weeks of moderate- to high-intensity exercise (n = 25) or treatment as usual (control group, n = 26), and CSF was collected before and after intervention. ResultsNo significant differences in CSF concentrations of VILIP-1, YKL-40, NFL, and Ng were observed when comparing mean change from baseline between the exercise and control groups. Similarly, when classifying subjects based on their exercise levels, no significant changes were observed for the biomarkers in the control group compared with the high-exercise group (attending 80% of the exercise sessions with an intensity of 70% of maximum heart rate or above). DiscussionThese results are not supportive of a modulatory effect of physical exercise on the selected biomarkers of neuronal and synaptic integrity in patients with AD.
Highlights
The molecular pathological mechanisms behind Alzheimer’s disease (AD) have been studied for decades
Elevated cerebrospinal fluid (CSF) Neurofilament light (NFL) is not a specific AD marker, and CSF NFL levels do not correlate with amyloid b 42 (Ab42) levels, indicating that the changes in NFL are not driven by Ab42 pathology [10]
There were no significant differences in baseline characteristics between control and intervention groups and in concentrations of visinin-like protein-1 (VILIP-1), NFL, Ng, and chitinase-3–like protein 1 (YKL-40) in CSF between the intervention group and control group (Table 1)
Summary
The molecular pathological mechanisms behind Alzheimer’s disease (AD) have been studied for decades. Jensen et al / Alzheimer’s & Dementia: Translational Research & Clinical Interventions 3 (2017) 284-290 studies in elderly suggest that participation in physical activity and cognitive training may reduce future cognitive decline [6] These studies have investigated possible effects on risk of dementia and cognitive decline in general and have not used any biomarkers to diagnose AD or study effects on AD pathophysiology. Apart from AD, increased levels have been found in CSF after stroke, other neurological disorders, and normal aging [14,15,16,17] This indicates that YKL-40 is more a general marker of neuroinflammation/astroglial activation secondary to many different etiologies, including Ab pathology [18]
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