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@ARTICLE{DaSilvaCorreia:281793,
author = {Da Silva Correia, Angela and Laginha, Ines and Guimaraes,
Susana and Dittmar, Kathrin and Schmitz, Matthias and
Castilla, Joaquin and Zerr, Inga and Silva-Correia, Susana},
title = {{P}edigree analysis and genetic inheritance of fatal
familial insomnia ({FFI}) in a {P}ortuguese
multigenerational family.},
journal = {Journal of neurology},
volume = {272},
number = {10},
issn = {0367-004X},
address = {[Darmstadt]},
publisher = {Steinkopff},
reportid = {DZNE-2025-01183},
pages = {706},
year = {2025},
abstract = {Fatal familial insomnia (FFI) is a rare, autosomal dominant
prion disease caused by a mutation in the PRNP gene, leading
to the misfolding of the cellular prion protein (PrPC) into
its pathogenic form (PrPSc). This results in
neurodegeneration, particularly in the thalamus, a key
region regulating sleep-wake cycles, which underlies the
hallmark symptoms of FFI, including insomnia, autonomic
dysfunctions, motor disturbances and cognitive decline. This
study focuses on a Portuguese family with FFI, providing a
detailed pedigree analysis spanning five generations and
comprising 134 individuals, to elucidate inheritance
patterns, disease onset, and clinical progression. The
findings confirm the autosomal-dominant inheritance pattern
and a strong familial clustering of the disease with age of
onset in the late 50s (mean 57 years). Although $67\%$ of
affected individuals succumbing to the disease within months
to 1.5 years, a notably $33\%$ exhibited prolonged survival
beyond the typical disease duration, exceeding proportions
reported in the literature. Family members retrospectively
reported prodromal symptoms, including generalized pain,
headaches, tinnitus, pruritus, and behavioral changes,
occurring up to five years before diagnosis. In several
cases, reportedly, disease onset was associated with major
phycological stressors (e.g., emotional stress or mourning).
While the significance of these observations remains
uncertain, they may provide insights into potential early
features in this kindred. Further research integrating
genomic sequencing, biomarkers, and longitudinal clinical
assessments are needed to better understand the mechanisms
underlying the heterogeneity of FFI and to explore potential
therapeutic interventions.},
keywords = {Humans / Insomnia, Fatal Familial: genetics / Insomnia,
Fatal Familial: physiopathology / Male / Middle Aged /
Portugal / Female / Pedigree / Adult / Prion Proteins:
genetics / Aged / Age of Onset / Disease Progression /
Extended Family / FFI (Other) / Fatal familial insomnia
(Other) / Portugal (Other) / PrPC (Other) / PrPSc (Other) /
Prion diseases (Other) / Prion Proteins (NLM Chemicals) /
PRNP protein, human (NLM Chemicals)},
cin = {AG Zerr},
ddc = {610},
cid = {I:(DE-2719)1440011-1},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41107634},
pmc = {pmc:PMC12534306},
doi = {10.1007/s00415-025-13432-2},
url = {https://pub.dzne.de/record/281793},
}