Aim:
Apathetic
syndrome is a common clinical feature in patients with Alzheimer
diseases (AD), from preclinical phases to late dementia stages, and it
is strongly related to major disease outcomes. Unfortunately,
no
specific pharmacological treatments for apathy have been accomplished so
far. Translational evidences have previously shown that a link between
apathy and hallmarks of AD-related pathophysiological, that is,
β-amyloid (Aβ) plaques, and neurofibrillary pathology exists. However,
only few studies investigated the association between cerebrospinal
fluid (CSF) core biomarkers of AD and apathy scores, finding conflicting
results.
Methods:
Thirty-seven
patients were identified as having AD dementia according to National
Institute on Aging–Alzheimer Association 2011 criteria. All participants
underwent an extensive diagnostic workup including CSF assessment to
assess the concentrations of the core biomarkers of AD pathophysiology,
that is, Aβ
42, t-tau, and pTau
181. To follow, they
were stratified as apathy absence, apathy mild, and apathy severe
according the score of the Neuro Psychiatric Inventory-apathy item. We
investigated for potential associations between apathy scores and CSF
core biomarkers concentrations as well as for differences in terms of
clinical and CSF biomarkers data across the 3 apathy groups.
Results:
The CSF Aβ
42 values were negatively correlated with apathy scores. In addition, patients with severe apathy had significantly lower Aβ
42 levels compared to nonapathetic ones.
Conclusion:
Based
on our results, we encourage further studies to untangle the potential
association between the complex pathophysiological dynamics of AD and
apathy. Apathy may represent an innovative reliable clinical outcome
measure to use in clinical trials, investigating treatments with either a
symptomatic or a disease-modifying effect.
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