Frontiers in Molecular Neuroscience 01 frontiersin.org
TYPE Brief Research Report
PUBLISHED 16 February 2023
DOI 10.3389/fnmol.2023.1104585
Co-occurring pathogenic variants
in 6q27 associated with dementia
spectrum disorders in a Peruvian
family
Karla Lucia F. Alvarez
1
, Jorge Alberto Aguilar-Pineda
1
,
Michelle M. Ortiz-Manrique
1
, Marluve F. Paredes-Calderon
2
,
Bryan C. Cardenas-Quispe
2
, Karin Jannet Vera-Lopez
1
,
Luis D. Goyzueta-Mamani
1
, Miguel Angel Chavez-Fumagalli
1
,
Gonzalo Davila-Del-Carpio
3
, Antero Peralta-Mestas
2
,
Patricia L. Musolino
4,5
and Christian Lacks Lino Cardenas
6
*
1
Laboratory of Genomics and Neurovascular Diseases, Universidad Católica de Santa María, Arequipa, Peru,
2
Division of Neurology, Psychiatry and Radiology of the National Hospital ESSALUD-HNCASE, Arequipa,
Peru,
3
Vicerrectorado de Investigación, Universidad Católica de Santa María, Arequipa, Peru,
4
Department of
Neurology, Massachusetts General Hospital, Boston, MA, United States,
5
Center for Genomic Medicine,
Massachusetts General Hospital, Boston, MA, United States,
6
Cardiovascular Research Center, Cardiology
Division, Massachusetts General Hospital, Boston, MA, United States
Evidence suggests that there may be racial diferences in risk factors associated
with the development of Alzheimer’s disease and related dementia (ADRD). We used
whole-genome sequencing analysis and identifed a novel combination of three
pathogenic variants in the heterozygous state (UNC93A: rs7739897 and WDR27:
rs61740334; rs3800544) in a Peruvian family with a strong clinical history of ADRD.
Notably, the combination of these variants was present in two generations of
afected individuals but absent in healthy members of the family. In silico and in vitro
studies have provided insights into the pathogenicity of these variants. These studies
predict that the loss of function of the mutant UNC93A and WDR27 proteins induced
dramatic changes in the global transcriptomic signature of brain cells, including
neurons, astrocytes, and especially pericytes and vascular smooth muscle cells,
indicating that the combination of these three variants may afect the neurovascular
unit. In addition, known key molecular pathways associated with dementia spectrum
disorders were enriched in brain cells with low levels of UNC93A and WDR27. Our
fndings have thus identifed a genetic risk factor for familial dementia in a Peruvian
family with an Amerindian ancestral background.
KEYWORDS
unbiased gene discovery, whole genome sequencing, family-specifc genetic factor,
Amerindian ancestral background, Alzheimer’s disease
1. Introduction
Neurological disorders are an important cause of disability and death around the world. Interestingly,
Alzheimer’s disease, dementia, Parkinson’s disease, epilepsy, schizophrenia, and autism spectrum
disorder share common anatomical alterations and cognitive defects (Kochunov et al., 2021). Certainly,
Alzheimer’s disease is the main cause of dementia, contributes 50 to 75% of cases (Report, 2021), and
can be presented in two forms as defned by age: early-onset Alzheimer’s disease (EOAD), which occurs
before 65 years of age, and late-onset Alzheimer’s disease (LOAD), which is mostly present afer 65 years
OPEN ACCESS
EDITED BY
Gal Bitan,
University of California,
Los Angeles,
United States
REVIEWED BY
Xiaopu Zhou,
Hong Kong University of Science and
Technology,
Hong Kong SAR, China
Maria Bullido,
Autonomous University of Madrid, Spain
*CORRESPONDENCE
Christian Lacks Lino Cardenas
clinocardenas@mgh.harvard.edu
SPECIALTY SECTION
This article was submitted to
Brain Disease Mechanisms,
a section of the journal
Frontiers in Molecular Neuroscience
RECEIVED 21 November 2022
ACCEPTED 18 January 2023
PUBLISHED 16 February 2023
CITATION
Alvarez KLF, Aguilar-Pineda JA,
Ortiz-Manrique MM, Paredes-Calderon MF,
Cardenas-Quispe BC, Vera-Lopez KJ,
Goyzueta-Mamani LD, Chavez-Fumagalli MA,
Davila-Del-Carpio G, Peralta-Mestas A,
Musolino PL and Lino Cardenas CL (2023)
Co-occurring pathogenic variants in 6q27
associated with dementia spectrum disorders
in a Peruvian family.
Front. Mol. Neurosci. 16:1104585.
doi: 10.3389/fnmol.2023.1104585
COPYRIGHT
© 2023 Alvarez, Aguilar-Pineda, Ortiz-
Manrique, Paredes-Calderon, Cardenas-
Quispe, Vera-Lopez, Goyzueta-Mamani,
Chavez-Fumagalli, Davila-Del-Carpio, Peralta-
Mestas, Musolino and Lino Cardenas. This is an
open-access article distributed under the terms
of the Creative Commons Attribution License
(CC BY). The use, distribution or reproduction
in other forums is permitted, provided the
original author(s) and the copyright owner(s)
are credited and that the original publication in
this journal is cited, in accordance with
accepted academic practice. No use,
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does not comply with these terms.