Tryptophan and nutritional status of patients with senile dementia

Thomas, Dawn; Chung-a-on, K.O.; Dickerson, J. W. T.; Tidmarsh, S. F.; Shaw, David M.

doi:10.1017/s0033291700009119

Cited by 29 publications

(17 citation statements)

References 27 publications

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“…A recent study showed patients with inflammatory diseases to have a significant depletion of serum levels of tryptophan compared to control population [23] and Huang et al demonstrated a clear relationship between reduced serum tryptophan levels and an increase of immune activation [24]. In addition, the decrease of the serum level of tryptophan was associated with cognitive deficit in senile dementias [25-27], and Noristani et al demonstrated that high triptophan diet lead to a reduction of the plaque pathology in Alzheimer's disease in mouse [28]. It is thus tempting to speculate that a microbiota-dependent reduction of tryptophan can nurture inflammaging in centenarians and could worsen the conditions of the patients affected by cognitive deficit.…”

Section: Discussionmentioning

confidence: 99%

Functional metagenomic profiling of intestinal microbiome in extreme ageing

Rampelli

Candela

Turroni

et al. 2013

Aging

296

220

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Age-related alterations in human gut microbiota composition have been thoroughly described, but a detailed functional description of the intestinal bacterial coding capacity is still missing. In order to elucidate the contribution of the gut metagenome to the complex mosaic of human longevity, we applied shotgun sequencing to total fecal bacterial DNA in a selection of samples belonging to a well-characterized human ageing cohort. The age-related trajectory of the human gut microbiome was characterized by loss of genes for shortchain fatty acid production and an overall decrease in the saccharolytic potential, while proteolytic functions were more abundant than in the intestinal metagenome of younger adults. This altered functional profile was associated with a relevant enrichment in “pathobionts”, i.e. opportunistic pro-inflammatory bacteria generally present in the adult gut ecosystem in low numbers. Finally, as a signature for long life we identified 116 microbial genes that significantly correlated with ageing. Collectively, our data emphasize the relationship between intestinal bacteria and human metabolism, by detailing the modifications in the gut microbiota as a consequence of and/or promoter of the physiological changes occurring in the human host upon ageing.

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Section: Discussionmentioning

confidence: 99%

Functional metagenomic profiling of intestinal microbiome in extreme ageing

Rampelli

Candela

Turroni

et al. 2013

Aging

296

220

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“…Two case2control studies reported lower blood levels of a nicotinic acid metabolite among demented patients than among age and sex matched controls. 12 13 We examined the association between dietary intake of niacin and tryptophan with incident AD and overall cognitive decline in a large prospective study of a biracial Chicago community.…”

mentioning

confidence: 99%

Dietary niacin and the risk of incident Alzheimer's disease and of cognitive decline

Morris

Evans²,

Bienias³

et al. 2004

Journal of Neurology, Neurosurgery & Psychiatry

173

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Background: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer's disease (AD) and cognitive decline in a large, prospective study. Methods: This study was conducted in 1993-2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical evaluations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria. Results: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (b = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (b = 0.023 SU/year; p = 0.02), or those with fewer than 12 years' education (b = 0.035 SU/year; p = 0.002) Conclusion: Dietary niacin may protect against AD and age related cognitive decline.

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“…Thomas et al [23] Severely demented patients (n = 23) and age-matched controls 3-day weighed intake Lower mean protein intake in the patient group. Also reduced plasma tryptophan concentrations.…”

Section: -Day Weighed Dietary Recordmentioning

confidence: 99%

“…In another study, performed with noncognitively impaired elderly persons, no difference in protein intake was observed between adequate and nonadequate scores on the MMSE and Pfeiffer's Mental Status Questionnaire (PMSQ) [20]. Three case-control studies were performed, of which two observed lower protein intakes in demented patients compared to age-matched controls [22,23]. The third study showed no difference in protein intake (Table 71.3) [24].…”

Section: Evidence From Observational Studiesmentioning

confidence: 99%