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Frailty syndrome in early‐onset autosomal dominant Alzheimer disease, in the PSEN1‐E280A kindred
Author(s) -
GarciaCifuentes Elkin,
Aguillon David,
Velez Juan Esteban,
Gómez Manuela,
GómezHenck Clara,
DeossaRestrepo Gloria,
Saldarriaga Jonathan,
JaramilloJimenez Alberto,
Ciro Jorge Alberto Osorio,
Borda Miguel German,
CanoGutierrez Carlos Alberto,
Lopera Francisco
Publication year - 2021
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.054704
Subject(s) - dementia , medicine , disease , psen1 , clinical dementia rating , neuropsychology , pediatrics , alzheimer's disease , gerontology , cognition , psychiatry , presenilin
Background Dementia has become a healthcare priority. As no disease‐modifying treatment is available, treatment is aimed to act through prevention. Frailty have been defined as a geriatric multidimensional syndrome. Being a treatable condition, interest has raised to describe the relationship between Dementia and Frailty. This study describes frailty in the Autosomal Dominant Alzheimer Disease, through the largest ADAD known group. Method A total of 75 participants (14 with MCI and 61 with Dementia) were included in this cross sectional study. They underwent a complete assessment that included a standardized clinical examination, neuropsychological evaluation and functional scales. Frailty was assessed through the Short Physical Performance Battery (SPPB) and the Time up and Go Test (TUG) . Multivariate analyses was conducted to evaluate which variables were associated with being frail in presenile onset of ADAD. Result In the 75 patients who underwent the study, median age was of 49 years old with a cognitive profile of 18.67 % individuals with MCI, 21 % with Mild, 28 % with Moderate and 25 % Severe Dementia. According to the frailty phenotype: 60 % were non‐frail and 40 % frail. When analyzing, SPPB and TUG components: Median Gait Speed in MCI and mild dementia groups were statistically significantly lower than moderate and severe dementia (p< 0.005) and significantly greater TUG was found in moderate and severe dementia groups when compared with MCI and mild dementia(p<0.005) Both, clinical severity grouped in moderate – severe dementia (OR 6.85; CI 2.07‐22.65 p< 0.000) and hypertension (OR 5.80; CI1.56‐21.49 <0.002) are significantly associated with being frail. Conclusion This study is the first description of frailty syndrome in ADAD with a presenile onset. The prevalence found in this population is similar than in previous reports in older adults and thus reasserts the adaptability of frailty evaluation in young patients with special clinical conditions. Our data supports the existing relationship between frailty and dementia. As the cause of dementia in our patients is purely genetic, effects of aging are controlled and excluded. This enrich science and lights up the search of new mechanisms linking both conditions.