Background In a previous study, higher concordance to the MIND diet, a hybrid Mediterranean-DASH diet, was associated with slower cognitive decline. In this study we related these three dietary patterns to incident Alzheimer’s disease. Methods We investigated the diet-AD relations in a prospective study of 923 participants, ages 58 to 98 years, followed on average 4.5 years. Diet was assessed by a semi-quantitative food frequency questionnaire. Results In adjusted proportional hazards models, the second (HR=0.65, 95% CI 0.44, 0.98) and highest tertiles (HR=0.47, 95% CI 0.26, 0.76) of MIND diet scores had lower rates of AD versus tertile 1 whereas only the third tertiles of the DASH (HR=0.61, 95% CI 0.38, 0.97) and Mediterranean (HR=0.46, 95% CI 0.26, 0.79) diets were associated with lower AD rates. Conclusion High adherence to all three diets may reduce AD risk. Moderate adherence to the MIND diet may also decrease AD risk.

Background The Mediterranean and DASH diets have been shown to slow cognitive decline, however, neither diet is specific to the nutrition literature on dementia prevention. Methods We devised the MIND diet score that specifically captures dietary components shown to be neuroprotective and related it to change in cognition over an average 4.7 years among 960 participants of the Memory and Aging Project. Results In adjusted mixed models, the MIND score was positively associated with slower decline in global cognitive score (β=0.0092; p<.0001) and with each of 5 cognitive domains. The difference in decline rates for being in the top tertile of MIND diet scores versus the lowest was equivalent to being 7.5 years younger in age. Conclusion The study findings suggest that the MIND diet substantially slows cognitive decline with age. Replication of these findings in a dietary intervention trial would be required to verify its relevance to brain health.

Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. The extent to which neuron loss in layer II of entorhinal cortex is related to mild cognitive impairment without dementia has not been extensively investigated. We analyzed 29 participants who came to autopsy from our ongoing longitudinal study of aging and dementia composed of religious clergy (Religious Orders Study). All individuals underwent detailed clinical evaluation within 12 months of death and were categorized as having no cognitive impairment (n = 8), mild cognitive impairment (n = 10), or mild or moderate Alzheimer's disease (n = 11). Sections through the entorhinal cortex were immunoreacted with an antibody directed against a neuron-specific nuclear protein (NeuN). Stereological counts of NeuN-immunoreactive stellate cells, their volume, and the volume of layer II entorhinal cortex were estimated. Cases exhibiting no cognitive impairment averaged 639,625 +/- 184,600 layer II stellate neurons in the right entorhinal cortex. Individuals with mild cognitive impairment (63.5%; p < 0.0003) and mild or moderate Alzheimer's disease (46.06%; p < 0.0017) displayed significant losses of layer II entorhinal cortex neurons relative to those with no cognitive impairment but not relative to each other (p > 0.33). There was also significant atrophy of layer II entorhinal cortex neurons in individuals with mild cognitive impairment (24.1%) and Alzheimer's disease (25.1%). The volume of layer II was also reduced in individuals with mild cognitive impairment (26.5%), with a further reduction in those with Alzheimer's disease (46.4%). The loss and atrophy of layer II entorhinal cortex neurons significantly correlated with performance on clinical tests of declarative memory. Atrophy of layer II entorhinal cortex and the neurons within this layer significantly correlated with performance on the Mini Mental Status Examination. These data indicate that atrophy and loss of layer II entorhinal cortex neurons occur in elderly subjects with mild cognitive impairment prior to the onset of dementia and suggests that these changes are not exacerbated in early Alzheimer's disease.

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