Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 12451340

[Late onset multiple sclerosis].

S Delalande·J De Seze·D Ferriby·T Stojkovic·P Vermersch
View original source ↗Export metadata ↓

Abstract

Multiple sclerosis (MS) with clinical onset after 50 years old is unusual and frequently misdiagnosed. Clinical presentation and course seem also to be different that in MS occurring between 20 and 50 years old. The aim of this study was to evaluate the clinical and paraclinical characteristics of late onset MS. We respectively studied MS patients older than 50 years at the onset of the disease. We evaluated demographical data, clinical symptoms, cerebrospinal fluid (CSF), visual evoked potentials (VEPs) and MRI of these patients. We also studied clinical data during the follow-up with the occurrence of new symptoms and the evolution of the disease by the index of progression (EDSS unit per year). In a population of 1 417 MS, 3.4 p.cent had their first symptoms at 50 years old or older and 0.45 p.cent after 59 years old. At the time of the study patients had more frequently a progressive form: 37 p.cent had a primary progressive form and 35 p.cent a secondary progressive MS. None of the patients with onset after 60 years old had relapsing remittent MS. Motor symptoms were the most common neurologic presentation (54 p.cent of patients). Very few patients had a clinical optic nerve involvement during the follow-up. The mean progression index was 1 suggesting a most severe evolution in this subgroup of MS patients. 76 p.cent of patients had oligoclonal banding detected by CSF electrophoresis. The VEPs were abnormal in 81 p. cent of patients tested. 71 p.cent of the brain MRI were consistent with the diagnosis of MS. 60 p.cent of patients had spinal cord MRI abnormal. This study highlights the differences between the late onset MS and earlier onset. As previously reported, our study underlines the high frequency of progressive course, motor function involvement and poor prognosis.

Explore related subjects

Age of OnsetAgedDiagnostic ErrorsDisease ProgressionElectrophoresisEvoked Potentials, VisualFemaleFollow-Up StudiesHumansImmunoglobulinsMaleMiddle AgedMultiple SclerosisOligoclonal BandsOptic NervePrognosisRetrospective StudiesSeverity of Illness IndexComparative StudyEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Delalande, J De Seze, D Ferriby, T Stojkovic, P Vermersch. 2002. [Late onset multiple sclerosis].. https://pubmed.ncbi.nlm.nih.gov/12451340/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2012

Role of genes linked to sporadic Alzheimer's disease risk in the production of β-amyloid peptides.

Alzheimer's disease (AD) is characterized by the presence of toxic protein aggregates or plaques composed of the amyloid β (Aβ) peptide. Various lengths of Aβ peptide are generated by proteolytic cleavages of the amyloid precursor protein (APP). Mutations in many familial AD-associated genes affect the production of the longer Aβ42 variant that preferentially accumulates in plaques. In the case of sporadic or late-onset AD, which accounts for greater than 95% of cases, several genes are implicated in increasing the risk, but whether they also cause the disease by altering amyloid levels is currently unknown. Through loss of function studies in a model cell line, here RNAi-mediated silencing of several late onset AD genes affected Aβ levels is shown. However, unlike the genes underlying familial AD, late onset AD-susceptibility genes do not specifically alter the Aβ42/40 ratios and suggest that these genes probably contribute to AD through distinct mechanisms.

Age of Onset↗
PubMed2012

Clinical and biomarker changes in dominantly inherited Alzheimer's disease.

BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.).

Age of Onset↗
PubMed2007

Follow-up mapping supports the evidence for linkage in the candidate region at 9q22 in the NIMH Alzheimer's disease Genetics Initiative cohort.

Other than the APOE peak at 19q13, the 9q22 region was identified in our original genomic scan as the candidate region with the highest multipoint lod score (MLS) in the subset of late onset Alzheimer's Disease (AD) families (MLS = 2.9 at 101 cM) from the NIMH Genetics Initiative sample. We have now genotyped an additional 12 short tandem repeats (STR) in this region. Multipoint analysis shows the region remains significant with an increase in the peak MLS from 2.9 to 3.8 at 95 cM near marker D9S1815, and the 1 LOD interval narrows from 21.5 to 11 cM. HLOD scores also provide evidence for significant linkage (4.5 with an alpha = 31%) with a further narrowing of the region to 6.6 cM (92.2-98.8 cM). Single nucleotide polymorphisms (SNPs) in the Ubiquilin1 gene (UBQLN1), located at 83.3 cM, have been reported to be significantly associated to AD, accounting for a substantial portion of the original linkage signal [Bertram et al., 2005]. Our analyses of the higher resolution genotype data generated here provide further support for the existence of a least one additional locus on chromosome 9q22. In an effort to pinpoint this putative AD susceptibility gene, we have begun to analyze SNPs in other candidate genes in and around this narrowed region to test for additional associations to AD.

Age of Onset↗