scholarly journals Clinical, pathophysiological and genetic features of motor symptoms in autosomal dominant Alzheimer’s disease

Brain ◽  
2019 ◽  
Vol 142 (5) ◽  
pp. 1429-1440 ◽  
Author(s):  
Jonathan Vöglein ◽  
Katrina Paumier ◽  
Mathias Jucker ◽  
Oliver Preische ◽  
Eric McDade ◽  
...  

Aβ deposition in the basal ganglia is common in autosomal dominant Alzheimer’s disease. Vöglein et al. report an increased severity of motor symptoms in autosomal dominant versus sporadic disease in advanced disease stages. Motor symptoms are more severe in post-codon 200 presenilin 1 mutation carriers and correlate with basal ganglia Aβ.

2017 ◽  
Vol 13 (7S_Part_15) ◽  
pp. P768-P769
Author(s):  
Nelly Joseph-Mathurin ◽  
Yi Su ◽  
Tyler Blazey ◽  
Mateusz S. Jasielec ◽  
Andrei G. Vlassenko ◽  
...  

2006 ◽  
Vol 14 (7S_Part_12) ◽  
pp. P650-P650
Author(s):  
Sidhartha Mahali ◽  
Simon Hsu ◽  
Bruno Benitez ◽  
Rita Martinez ◽  
Alison M. Goate ◽  
...  

2021 ◽  
Vol 10 (19) ◽  
pp. 4582
Author(s):  
Tanzil Rujeedawa ◽  
Eva Carrillo Félez ◽  
Isabel C. H. Clare ◽  
Juan Fortea ◽  
Andre Strydom ◽  
...  

The purpose of this review is to compare and highlight the clinical and pathological aspects of genetic versus acquired Alzheimer’s disease: Down syndrome-associated Alzheimer’s disease in (DSAD) and Autosomal Dominant Alzheimer’s disease (ADAD) are compared with the late-onset form of the disease (LOAD). DSAD and ADAD present in a younger population and are more likely to manifest with non-amnestic (such as dysexecutive function features) in the prodromal phase or neurological features (such as seizures and paralysis) especially in ADAD. The very large variety of mutations associated with ADAD explains the wider range of phenotypes. In the LOAD, age-associated comorbidities explain many of the phenotypic differences.


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