Age‐associated memory impairment: Proposed diagnostic criteria and measures of clinical change — report of a national institute of mental health work group

Crook, Thomas H.; Bartus, Raymond T.; Ferris, Steven H.; Whitehouse, Peter J.; Cohen, Gene D.; Gershon, Samuel

doi:10.1080/87565648609540348

Cited by 843 publications

(480 citation statements)

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“…We used a validated Spanish version ranging from 0 to 7 (del Ser Quijano et al 2004). Both cognitive tests are valid indicators of cognitive impairment (Crook et al 1986;Paganini-Hill and Clark 2011). Researchers who assessed the outcome were blinded to group assignment.…”

Section: Cognitive Assessmentmentioning

confidence: 99%

Genotype patterns at CLU, CR1, PICALM and APOE, cognition and Mediterranean diet: the PREDIMED-NAVARRA trial

et al. 2014

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The traditional Mediterranean diet (MedDiet) has shown beneficial effects on cognitive decline. Nevertheless, diet-gene interactions have been poorly evaluated. We aimed to investigate diet-gene interaction in the PREDIMED-NAVARRA randomized trial. A total of 522 participants (67 ± 6 years at baseline) enrolled in the PREDIMED-NAVARRA trial were randomly allocated to one of three diets: two MedDiets (supplemented with either extra-virgin olive oil or nuts) or a low-fat diet. They were evaluated with the Mini-Mental State Examination (MMSE) and the Clock Drawing Test (CDT) after 6.5 years of intervention. Subjects were genotyped for CR1-rs3818361, CLU-rs11136000, PICALM-rs3851179 and Apolipoprotein E (ApoE) genes. We studied MedDietgene interactions for cognition and assessed the effect of the MedDiet on cognition across different genetic profiles. A significant interaction (p = 0.041) between CLUrs11136000 and the MedDiet intervention on the MMSE was found with a beneficial effect of MedDiet among carriers of the T minor allele (B = 0.97, 95 % CI 0.45-1.49). Similar effect was observed for CR1-rs3818361, but no significant interaction was observed (p = 0.335). For PICALM-rs3851179, the MedDiet intervention showed a beneficial effect in both genotype groups. No apparent interaction was found for the CDT between intervention and gene variants. Similarly, participants randomly allocated to MedDiet groups, with favorable 123Genes Nutr (2014) 9:393 DOI 10.1007/s12263-014-0393-7 profiles of CR1, CLU and PICALM genes, significantly improved CDT scores compared to controls with the same genetic profile. Cognitive performance was better for nonApoE4 and for ApoE4 carriers of MedDiet groups compared to controls, but for CDT performance, we only found statistical significant differences for non-ApoE4 carriers. A MedDiet intervention modulates the effect of genetic factors on cognition. The effect of MedDiet might be greater for subjects with a more favorable genetic profile.

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Section: Cognitive Assessmentmentioning

confidence: 99%

Genotype patterns at CLU, CR1, PICALM and APOE, cognition and Mediterranean diet: the PREDIMED-NAVARRA trial

et al. 2014

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“…Age-related decline in learning and memory, often termed age-associated memory impairment (AAMI) (Crook et al, 1986), is a well-documented finding in healthy older adults (Balota et al, 2000;Cabeza et al, 2000;Craik, 1994;Salthouse, 2003), but the neurobiological correlates of this decline are still under debate. A consistent pattern of AAMI is a decrement in declarative memory (Tulving, 1985) most clearly apparent in impaired free recall and recollection (Buckner, 2004;Craik, 2006;Hedden and Gabrieli, 2004;Nilsson, 2003).…”

Section: Introductionmentioning

confidence: 99%

Basal forebrain integrity and cognitive memory profile in healthy aging

Düzel¹,

Münte²,

Lindenberger³

et al. 2010

Brain Research

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Age-related dysfunctions in cholinergic and dopaminergic neuromodulation are assumed to contribute to age-associated impairment of explicit memory. Both neurotransmitters also modulate attention, working memory, and processing speed. To date, in vivo evidence linking structural age-related changes in these neuromodulatory systems to dysfunction within or across these cognitive domains remains scarce. Using a factor analytical approach in a cross-sectional study including 86 healthy older (aged 55 to 83 years) and 24 young (aged 18 to 30 years) adults, we assessed the relationship between structural integrity-as measured by magnetization transfer ratio (MTR)-of the substantia nigra/ventral tegmental area (SN/VTA), main origin of dopaminergic projections, basal forebrain (major origin of cortical cholinergic projections), frontal white matter (FWM), and hippocampus to neuropsychological and psychosocial scores. Basal forebrain MTR and FWM changes correlated with a factor combining verbal learning and memory and working memory and, as indicated by measures of diffusion, were most likely due to vascular pathology. These findings suggest that frontal white matter integrity and cholinergic neuromodulation provide clues as to why age-related cognitive decline is often correlated across cognitive domains. IntroductionAge-related decline in learning and memory, often termed age-associated memory impairment (AAMI) (Crook et al., 1986), is a well-documented finding in healthy older adults (Balota et al., 2000;Cabeza et al., 2000;Craik, 1994;Salthouse, 2003), but the neurobiological correlates of this decline are still under debate. A consistent pattern of AAMI is a decrement in declarative memory (Tulving, 1985) most clearly apparent in impaired free recall and recollection (Buckner, 2004;Craik, 2006;Hedden and Gabrieli, 2004;Nilsson, 2003). Evidence from lesion studies in humans and animals indicates that

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“…En effet, le diagnostic de maladie d'Alzheimer ne doit être porté que chez un patient dit « dément », c'est-à-dire chez un patient qui a perdu son autonomie [3]. Le spectre des troubles cognitifs se trouve donc interrompu en son milieu, entre, à une extrémité, les troubles cognitifs associés à l'âge (qui se sont successivement appelés : oubli bénin de l'âge [4] ; age associated memory impairment -AAMI [5] ; age associated cognitive decline -AACD [6] et age related cognitive decline -ARCD [7]) et à l'autre l'extrémité, les troubles cognitifs démentiels, quelle qu'en soit l'étiologie : vasculaire, dégénérative... MEDECINE/SCIENCES 2002 ;18 : 775-9 FORUM HYPOTHÈSES ET DÉBATS > Avant la démence, la maladie d'Alzheimer est déjà à l'oeuvre dans le cerveau. Les données neuropathologiques et biochimiques récentes indiquent que les lésions neuronales intéressent, aux stades pré-démentiels, les structures temporales internes (formation hippocampique, gyrus para-hippocampique, cortex entorhinal) dont on connaît le rôle dans la mémorisation à long terme.…”

unclassified

Avant la démence…, ou les limites du concept de trouble cognitif léger (MCI : mild cognitive impairment)

2002

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Age‐associated memory impairment: Proposed diagnostic criteria and measures of clinical change — report of a national institute of mental health work group

Cited by 843 publications

References 24 publications

Genotype patterns at CLU, CR1, PICALM and APOE, cognition and Mediterranean diet: the PREDIMED-NAVARRA trial

Genotype patterns at CLU, CR1, PICALM and APOE, cognition and Mediterranean diet: the PREDIMED-NAVARRA trial

Basal forebrain integrity and cognitive memory profile in healthy aging

Avant la démence…, ou les limites du concept de trouble cognitif léger (MCI : mild cognitive impairment)

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