Faculty Opinions recommendation of Cortical atrophy accelerates as cognitive decline worsens in multiple sclerosis.

ObjectiveTo determine which pathologic process could be responsible for the acceleration of cognitive decline during the course of multiple sclerosis (MS), using longitudinal structural MRI, which was related to cognitive decline in relapsing-remitting MS (RRMS) and progressive MS (PMS).MethodsA prospective cohort of 230 patients with MS (179 RRMS and 51 PMS) and 59 healthy controls was evaluated twice with 5-year (mean 4.9, SD 0.94) interval during which 22 patients with RRMS converted to PMS. Annual rates of cortical and deep gray matter atrophy as well as lesion volume increase were computed on longitudinal (3T) MRI data and correlated to the annual rate of cognitive decline as measured using an extensive cognitive evaluation at both time points.ResultsThe deep gray matter atrophy rate did not differ between PMS and RRMS (−0.82%/year vs −0.71%/year, p = 0.11), while faster cortical atrophy was observed in PMS (−0.87%/year vs −0.48%/year, p < 0.01). Similarly, faster cognitive decline was observed in PMS compared to RRMS (p < 0.01). Annual cognitive decline was related to the rate of annual lesion volume increase in stable RRMS (r = −0.17, p = 0.03) to the rate of annual deep gray matter atrophy in converting RRMS (r = 0.50, p = 0.02) and annual cortical atrophy in PMS (r = 0.35, p = 0.01).ConclusionsThese results indicate that cortical atrophy and cognitive decline accelerate together during the course of MS. Substrates of cognitive decline shifted from worsening lesional pathology in stable RRMS to deep gray matter atrophy in converting RRMS and to accelerated cortical atrophy in PMS only.

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Whole Brain Tract Disruption Better Explains Cognitive Decline in Multiple Sclerosis than Total Lesion Volume

10.26226/morressier.59a3e8b7d462b8028d895711 ◽

2017 ◽

Author(s):

Tom Fuchs

Keyword(s):

Multiple Sclerosis ◽

Cognitive Decline ◽

Lesion Volume ◽

Whole Brain

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Faculty Opinions recommendation of Cognitive reserve and cortical atrophy in multiple sclerosis: a longitudinal study.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717999376.793475377 ◽

2013 ◽

Author(s):

Massimo Filippi ◽

Maria Rocca

Keyword(s):

Multiple Sclerosis ◽

Longitudinal Study ◽

Cognitive Reserve ◽

Cortical Atrophy

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Cognitive Issues in Pediatric Multiple Sclerosis

Brain Sciences ◽

10.3390/brainsci11040442 ◽

2021 ◽

Vol 11 (4) ◽

pp. 442

Author(s):

Emilio Portaccio ◽

Ermelinda De Meo ◽

Angelo Bellinvia ◽

Maria Pia Amato

Keyword(s):

Multiple Sclerosis ◽

Cognitive Impairment ◽

Cognitive Decline ◽

Pediatric Patients ◽

Leisure Activities ◽

Disease Onset ◽

Cognitive Profiles ◽

Brain Growth ◽

Network Activation ◽

Definition Of

Multiple sclerosis (MS) is one of the leading causes of disability in young adults. The onset of MS during developmental age makes pediatric patients particularly susceptible to cognitive impairment, resulting from both disease-related damage and failure of age-expected brain growth. Despite different test batteries and definitions, cognitive impairment has been consistently reported in approximately one-third of pediatric patients with MS. However, the lack of a uniform definition of cognitive impairment and the adoption of different test batteries have led to divergent results in terms of cognitive domains more frequently affected across the cohorts explored. This heterogeneity has hampered large international collaborative studies. Moreover, research aimed at the identification of risk factors (e.g., demographic, clinical, and radiological features) or protective factors (e.g., cognitive reserve, leisure activities) for cognitive decline is still scanty. Mood disorders, such as depression and anxiety, can be detected in these patients alongside cognitive decline or in isolation, and can negatively affect quality of life scores as well as academic performances. By using MRI, cognitive impairment was attributed to damage to specific brain compartments as well as to abnormal network activation patterns. However, multimodal MRI studies are still needed in order to assess the contribution of each MRI metric to cognitive impairment. Importantly, longitudinal studies have recently demonstrated failure of age-expected brain growth and of white matter (WM) and gray matter (GM) maturation plays a relevant role in determining cognitive dysfunction, in addition to MS-related direct damage. Whether these growth retardations might result in specific cognitive profiles according to the age at disease onset has not been studied, yet. A better characterization of cognitive profiles in pediatric MS patients, as well as the definition of neuroanatomical substrates of cognitive impairment and their longitudinal evolution are needed to develop efficient therapeutic strategies against cognitive impairment in this patient population.

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Cortical Thinning Associated with Age and CSF Biomarkers in Early Parkinson’s Disease Is Modified by the SNCA rs356181 Polymorphism

Neurodegenerative Diseases ◽

10.1159/000493103 ◽

2018 ◽

Vol 18 (5-6) ◽

pp. 233-238

Author(s):

Frederic Sampedro ◽

Juan Marín-Lahoz ◽

Saul Martínez-Horta ◽

Javier Pagonabarraga ◽

Jaime Kulisevsky

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cognitive Decline ◽

De Novo ◽

Brain Regions ◽

Cortical Atrophy ◽

Csf Biomarkers ◽

Gene Encoding ◽

Cortical Thinning ◽

Age Related

The role of cerebrospinal fluid (CSF) biomarkers such as CSF α-synuclein and CSF tau in predicting cognitive decline in Parkinson’s disease (PD) continues to be inconsistent. Here, using a cohort of de novo PD patients with preserved cognition from the Parkinson’s Progression Markers Initiative (PPMI), we show that the SNCA rs356181 single nucleotide polymorphism (SNP) modulates the effect of these CSF biomarkers on cortical thinning. Depending on this SNP’s genotype, cortical atrophy was associated with either higher or lower CSF biomarker levels. Additionally, this SNP modified age-related atrophy. Importantly, the integrity of the brain regions where this phenomenon was observed correlated with cognitive measures. These results suggest that this genetic variation of the gene encoding the α-synuclein protein, known to be involved in the development of PD, also interferes in its subsequent neurodegeneration. Overall, our findings could shed light on the so far incongruent association of common CSF biomarkers with cognitive decline in PD.

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Cognitive reserve in elderly: neuropsychological aspects and the education role in the latest findings

Revista de Medicina ◽

10.11606/issn.1679-9836.v94i3p136-146 ◽

2015 ◽

Vol 94 (3) ◽

pp. 136

Author(s):

João Gabriel Magalhães Dias ◽

Pablo Rodrigo Andrade da Silva ◽

Tânia Corrêa de Toledo Ferraz Alvez

Keyword(s):

Executive Function ◽

Cognitive Decline ◽

Cognitive Performance ◽

Cognitive Abilities ◽

Elderly Population ◽

Cognitive Reserve ◽

The Elderly ◽

Cortical Atrophy ◽

Print Exposure ◽

Cognitive Markers

The elderly population is growing worldwide, and therefore cognitive decline and dementia is a major problem for healthcare system. However, many elders do not develop dementia or significant cognitive impairment even though present brain lesions, such as cortical atrophy and/or lesions, leading to the concept of Cognitive Reserve (CR). The main objective of this review is to establish the recent findings of CR in elderly cognition and explore some of the cognitive markers related to CR. In order to accomplish that we carried out a search for papers published either in English or Portuguese language in the last 5 years in the Medline database using as keywords cognitive reserve, elderly and aging/ageing. We filtered 14 studies that specifically approached the neuropsychological aspects (e.g, memory, attention, orientation, executive function) and reviewed them in detail. Based on these papers regarding old-aged individuals, education appears to have several implications on CR by strengthening cognitive abilities, however does not appear to impact on cognitive decline. Besides, we realized that cognitive performance is one of the form to measure CR, even though the methods cannot be standardized, which may be the cause of some varied conclusions. Regarding CR, education was the most prevalent measure, and CR seems to have a beneficial effect on executive function and episodic memory and it seems to act by both neural reserve and neural compensation. Print exposure appears as a potential variable positively related to cognitive performance and CR.

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Cognitive reserve and cortical atrophy in multiple sclerosis: A longitudinal study

Neurology ◽

10.1212/wnl.0b013e3182918c6f ◽

2013 ◽

Vol 80 (19) ◽

pp. 1728-1733 ◽

Cited By ~ 78

Author(s):

M. P. Amato ◽

L. Razzolini ◽

B. Goretti ◽

M. L. Stromillo ◽

F. Rossi ◽

...

Keyword(s):

Multiple Sclerosis ◽

Longitudinal Study ◽

Cognitive Reserve ◽

Cortical Atrophy

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Cognitive reserve moderates the impact of subcortical gray matter atrophy on neuropsychological status in multiple sclerosis

Multiple Sclerosis Journal ◽

10.1177/1352458515579443 ◽

2015 ◽

Vol 22 (1) ◽

pp. 36-42 ◽

Cited By ~ 39

Author(s):

Claire M Modica ◽

Niels Bergsland ◽

Michael G Dwyer ◽

Deepa P Ramasamy ◽

Ellen Carl ◽

...

Keyword(s):

Multiple Sclerosis ◽

Cognitive Decline ◽

Cognitive Processing ◽

Gray Matter ◽

Cognitive Reserve ◽

Cognitive Outcome ◽

Brain Reserve ◽

The Impact ◽

Normal Controls

Background: Cognitive decline is characterized in multiple sclerosis (MS), but the rate and severity vary. The reserve hypothesis proposes that baseline neurological differences impact cognitive outcome in neurodegenerative disease. Objective: To elucidate how brain reserve and cognitive reserve influence subcortical gray matter (SCGM) atrophy and cognitive decline in MS over 3 years. Methods: Seventy-one MS patients and 23 normal controls underwent magnetic resonance imaging and cognitive assessment at baseline and 3-year follow-up. The influence of reserve on cognitive processing speed (CPS) and memory was examined. Results: SCGM volume and cognitive scores were lower in MS than normal controls ( P⩽0.001). Accounting for baseline, comparison of follow-up means yielded a difference between groups in SCGM volume ( P<0.001) but not cognition (NS). Cognitive reserve ( P=0.005), but not brain reserve, contributed to CPS, with only low cognitive reserve MS subjects showing decline in CPS ( P=0.029). SCGM change predicted CPS outcome in MS with low cognitive reserve ( P=0.002) but not high cognitive reserve. There were no effects in the domain of memory. Conclusions: SCGM atrophy occurs in normal controls, but significantly more so in MS. While CPS did not change in normal controls, low cognitive reserve was associated with CPS decline in MS. High cognitive reserve protect MS patients from cognitive decline related to SCGM atrophy.

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