Differences in Routine Clinical Practice between Early and Late Onset Alzheimer's Disease: Data from the Swedish Dementia Registry (SveDem)

2014 ◽  
Vol 41 (2) ◽  
pp. 411-419 ◽  
Author(s):  
Hanna Eriksson ◽  
Seyed-Mohammad Fereshtehnejad ◽  
Farshad Falahati ◽  
Bahman Farahmand ◽  
Dorota Religa ◽  
...  
2009 ◽  
Vol 5 (4S_Part_12) ◽  
pp. P353-P353 ◽  
Author(s):  
Audrey Gabelle ◽  
Stéphane Roche ◽  
Christian Geny ◽  
Jacques Touchon ◽  
Sylvain Lehmann

2017 ◽  
Vol 2017 ◽  
pp. 1-6
Author(s):  
Luca Rozzini ◽  
Anna Ceraso ◽  
Marina Zanetti ◽  
Silvia Pelizzari ◽  
Evita Tomasoni ◽  
...  

Background. The five-word test (FWT) is a neuropsychological tool (derived from the Grober and Buschke paradigm), measuring hippocampal memory trace consolidation. The study aimed to validate the test for the Italian language and to verify its ability to discriminate patients affected by mild cognitive impairment and dementia due to Alzheimer’s disease from healthy matches. Methods. 217 subjects (127 controls, 47 MCI due to AD, and 43 AD) underwent neuropsychological evaluation. The Spearman rank coefficient (ρ) was used to assess the correlation between immediate (IRS), delayed (DRS), and total score (TRS) of the FWT and correspondent matches of a specific short story test, while receiving operator characteristic (ROC) curves were built to investigate the diagnostic accuracy of both. Results. Correlation between almost all the scores was significant in all the diagnostic subgroups; the ROC curves of the two tests were not statistically different. A TRS of the FWT with a cut-off of ≤9/10 could accurately discriminate AD patients (sensitivity: 97%, specificity: 94%) and MCI due to AD (sensitivity: 76%, specificity: 68%) from control matches. Conclusion. FWT is a simple and valid test of hippocampal memory which appears recommendable in routine clinical practice.


2021 ◽  
pp. 1-17
Author(s):  
Mandy Melissa Jane Wittens ◽  
Diana Maria Sima ◽  
Ruben Houbrechts ◽  
Annemie Ribbens ◽  
Ellis Niemantsverdriet ◽  
...  

Background: Magnetic resonance imaging (MRI) has become important in the diagnostic work-up of neurodegenerative diseases. icobrain dm, a CE-labeled and FDA-cleared automated brain volumetry software, has shown potential in differentiating cognitively healthy controls (HC) from Alzheimer’s disease (AD) dementia (ADD) patients in selected research cohorts. Objective: This study examines the diagnostic value of icobrain dm for AD in routine clinical practice, including a comparison to the widely used FreeSurfer software, and investigates if combined brain volumes contribute to establish an AD diagnosis. Methods: The study population included HC (n = 90), subjective cognitive decline (SCD, n = 93), mild cognitive impairment (MCI, n = 357), and ADD (n = 280) patients. Through automated volumetric analyses of global, cortical, and subcortical brain structures on clinical brain MRI T1w (n = 820) images from a retrospective, multi-center study (REMEMBER), icobrain dm’s (v.4.4.0) ability to differentiate disease stages via ROC analysis was compared to FreeSurfer (v.6.0). Stepwise backward regression models were constructed to investigate if combined brain volumes can differentiate between AD stages. Results: icobrain dm outperformed FreeSurfer in processing time (15–30 min versus 9–32 h), robustness (0 versus 67 failures), and diagnostic performance for whole brain, hippocampal volumes, and lateral ventricles between HC and ADD patients. Stepwise backward regression showed improved diagnostic accuracy for pairwise group differentiations, with highest performance obtained for distinguishing HC from ADD (AUC = 0.914; Specificity 83.0%; Sensitivity 86.3%). Conclusion: Automated volumetry has a diagnostic value for ADD diagnosis in routine clinical practice. Our findings indicate that combined brain volumes improve diagnostic accuracy, using real-world imaging data from a clinical setting.


2003 ◽  
Author(s):  
J. M. Silverman ◽  
C. J. Smith ◽  
D. B. Marin ◽  
R. C. Mohs ◽  
C. B. Propper

2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.


2020 ◽  
Vol 20 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Sharifa Hasana ◽  
Md. Farhad Hossain ◽  
Md. Siddiqul Islam ◽  
Tapan Behl ◽  
...  

: Alzheimer’s disease (AD) is the most common form of dementia in the elderly and this complex disorder is associated with environmental as well as genetic components. Early-onset AD (EOAD) and late-onset AD (LOAD, more common) are major identified types of AD. The genetics of EOAD is extensively understood with three genes variants such as APP, PSEN1, and PSEN2 leading to disease. On the other hand, some common alleles including APOE are effectively associated with LOAD identified but the genetics of LOAD is not clear to date. It has been accounted that about 5% to 10% of EOAD patients can be explained through mutations in the three familiar genes of EOAD. The APOE ε4 allele augmented the severity of EOAD risk in carriers, and APOE ε4 allele was considered as a hallmark of EOAD. A great number of EOAD patients, who are not genetically explained, indicate that it is not possible to identify disease- triggering genes yet. Although several genes have been identified through using the technology of next-generation sequencing in EOAD families including SORL1, TYROBP, and NOTCH3. A number of TYROBP variants were identified through exome sequencing in EOAD patients and these TYROBP variants may increase the pathogenesis of EOAD. The existence of ε4 allele is responsible for increasing the severity of EOAD. However, several ε4 allele carriers live into their 90s that propose the presence of other LOAD genetic as well as environmental risk factors that are not identified yet. It is urgent to find out missing genetics of EOAD and LOAD etiology to discover new potential genetics facets which will assist to understand the pathological mechanism of AD. These investigations should contribute to developing a new therapeutic candidate for alleviating, reversing and preventing AD. This article based on current knowledge represents the overview of the susceptible genes of EOAD, and LOAD. Next, we represent the probable molecular mechanism which might elucidate the genetic etiology of AD and highlight the role of massively parallel sequencing technologies for novel gene discoveries.


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