Premium
Hypertension accentuates reductions in CSF Aβ42 in elderly depressives
Author(s) -
Pomara Nunzio,
Bruno Davide,
Reichert Chelsea,
Lee Sang Han,
Sarreal Antero,
Hernando Raymundo,
RamosCejudo Jaime,
Zetterberg Henrik,
Blennow Kaj
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.046299
Subject(s) - medicine , dementia , depression (economics) , cohort , disease , hyperintensity , apolipoprotein e , risk factor , cardiology , endocrinology , magnetic resonance imaging , radiology , economics , macroeconomics
Background Hypertension (HTN) is a well‐established risk factor for Alzheimer’s disease (AD). Observations from animal and human PET studies indicate that HTN may be mechanistically linked to AD by increasing brain Aβ deposition which may represent the first pathogenetic event in the onset of AD dementia. For example, a diagnosis of HTN, has been associated with increased brain Aβ on PET imaging in humans. HTN is also common in late‐life depression (LLMD), a disorder which is also associated with increased risk for AD and altered Aβ dynamics consistent with increased brain Aβ burden including reductions in CSF Aβ42. Our group first reported a reduction in CSF Aβ42 which was unrelated to APOE status. However, the neurobiological mechanisms for the association between LLMD and altered Aβ metabolism are not fully understood and might involve co‐morbid vascular factors such as HTN. These considerations prompted us to examine the relationship between LLMD, HTN and CSF AD biomarkers in a cohort of non‐demented elderly. Methods CSF was obtained from 47 individuals (28‐LLMD and 19 ‐controls) 60 years or older with MMSE>28 and without significant white matter hyperintensities. A general linear model was used to compare the effect of hypertension status (HTN; Hypertensive or Not Hypertensive) and diagnosis (Dx; LLMD or control) on baseline AD biomarkers (Aβ42, Aβ40). Results We found that controls without HTN (mean=361 pg/ml) had sig. higher CSF Aβ42 than LLMD without HTN (mean=220 pg/ml; Tukey adj. p‐value = 0.18) and LLMD with HTN (mean=202 pg/ml; Tukey adj. p‐value = .031) given the significant interaction of HTN and Dx (p=0.05). There was also a main effect of HTN on Aβ40 (p=.025). Conclusions These preliminary results suggest that hypertension and LLMD are independently associated with reductions in CSF Aβ42 and that co‐morbid HTN may accentuate its reduction in LLMD. Thus, more effective treatment of depression and HTN may attenuate the increased risk for AD associated with these disorders.