According to the Cognitive reserve hypothesis, several factors related to mental engagement, such as level of education, type of occupation, leisure activities and social network, appear to affect the risk of developing clinical dementia. The present article provides an overview of the studies that have investigated the effects of mental engagement and cognitive stimulation specifically on dementia of the Alzheimer’s type (AD). Mental training and cognitive stimulation interventions in AD have been shown to be useful in increasing patients’ ability in performing activities of daily living (ADL), allowing them to maintain relative independence. Since cognitive engagement and stimulation are known to modify the brain processes to perform tasks, by recruiting alternative and more efficient networks, this review is especially focused on cognitive rehabilitation in AD patients, which has been shown to improve their global functioning and cognition. This perspective stresses the idea that cognitive reserve is not a fixed factor, but can be continuously modified by life experiences, even when the brain is already affected by neuropathology.

Liberati G, Raffone A, Olivetti Belardinelli M.
Interuniversity Centre for Research on Cognitive Processing in Natural and Artificial Systems (ECONA), IT, Rome, Italy.

Cochrane Database Syst Rev. 2011 Jan 19;1:CD006220.

Martin M, Clare L, Altgassen AM, Cameron MH, Zehnder F.
Psychologisches Institut, Universität Zürich, Lehrstuhl Gerontopsychologie, Binzmühlestrasse 14/24, Zürich, Switzerland, CH-8050.
Abstract
BACKGROUND: Evidence from some, but not all non-randomised studies suggest the possibility that cognitive training may influence cognitive functioning in older people. Due to the differences among cognitive training interventions reported in the literature, giving a general overview of the current literature remains difficult.
OBJECTIVES: To systematically review the literature and summarize the effect of cognitive training interventions on various domains of cognitive function (ie memory, executive function, attention and speed) in healthy older people and in people with mild cognitive impairment.
SEARCH STRATEGY: The CDCIG Specialized Register was searched on 30 September 2007 for all years up to December 2005. The Cochrane Library, MEDLINE, EMBASE, PsycINFO and CINAHL were searched separately on 30 September 2007 to find trials with healthy people. These results were supplemented by searches from January 1970 to September 2007 in PsychInfo/Psyndex, ISI Web of Knowledge and PubMed.
SELECTION CRITERIA: RCTs of interventions evaluating the effectiveness of cognitive training for healthy older people and people with mild cognitive impairment from 1970 to 2007 that met inclusion criteria were selected.
DATA COLLECTION AND ANALYSIS: Authors independently extracted data and assessed trial quality. Meta-analysis was performed when appropriate.
MAIN RESULTS: Only data on memory training could be pooled for analysis. Within this domain, training interventions were grouped according to several outcome variables. Results showed that for healthy older adults, immediate and delayed verbal recall improved significantly through training compared to a no-treatment control condition. We did not find any specific memory training effects though as the improvements observed did not exceed the improvement in the active control condition. For individuals with mild cognitive impairment, our analyses demonstrate the same pattern. Thus, there is currently little evidence on the effectiveness and specificity of memory interventions for healthy older adults and individuals with mild cognitive impairment.
AUTHORS’ CONCLUSIONS: There is evidence that cognitive interventions do lead to performance gains but none of the effects observed could be attributable specifically to cognitive training, as the improvements observed did not exceed the improvement in active control conditions. This does not mean that longer, more intense or different interventions might not be effective, but that those which have been reported thus far have only limited effect. We therefore suggest more standardized study protocols in order to maximize comparability of studies and to maximize the possibility of data pooling – also in other cognitive domains than memory.

Arch Neurol. 2011 Feb;68(2):214-20.

Lin FR, Metter EJ, O’Brien RJ, Resnick SM, Zonderman AB, Ferrucci L.
Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins School of Medicine, JHOC 6120, 601 N Caroline St, Baltimore, MD 21287. flin1@jhmi.edu.
Abstract
OBJECTIVE: To determine whether hearing loss is associated with incident all-cause dementia and Alzheimer disease (AD).
DESIGN: Prospective study of 639 individuals who underwent audiometric testing and were dementia free in 1990 to 1994. Hearing loss was defined by a pure-tone average of hearing thresholds at 0.5, 1, 2, and 4 kHz in the better-hearing ear (normal, <25 dB [n = 455]; mild loss, 25-40 dB [n = 125]; moderate loss, 41-70 dB [n = 53]; and severe loss, >70 dB [n = 6]). Diagnosis of incident dementia was made by consensus diagnostic conference. Cox proportional hazards models were used to model time to incident dementia according to severity of hearing loss and were adjusted for age, sex, race, education, diabetes mellitus, smoking, and hypertension.
SETTING: Baltimore Longitudinal Study of Aging.
PARTICIPANTS: Six hundred thirty-nine individuals aged 36 to 90 years. Main Outcome Measure  Incident caces of all-cause dementia and AD until May 31, 2008.
RESULTS: During a median follow-up of 11.9 years, 58 cases of incident all-cause dementia were diagnosed, of which 37 cases were AD. The risk of incident all-cause dementia increased log linearly with the severity of baseline hearing loss (1.27 per 10-dB loss; 95% confidence interval, 1.06-1.50). Compared with normal hearing, the hazard ratio (95% confidence interval) for incident all-cause dementia was 1.89 (1.00-3.58) for mild hearing loss, 3.00 (1.43-6.30) for moderate hearing loss, and 4.94 (1.09-22.40) for severe hearing loss. The risk of incident AD also increased with baseline hearing loss (1.20 per 10 dB of hearing loss) but with a wider confidence interval (0.94-1.53).
CONCLUSIONS: Hearing loss is independently associated with incident all-cause dementia. Whether hearing loss is a marker for early-stage dementia or is actually a modifiable risk factor for dementia deserves further study

Neuroimage. 2011 Jan 31. [Epub ahead of print]

Almeida OP, Garrido GJ, Alfonso H, Hulse G, Lautenschlager NT, Hankey GJ, Flicker L.
Western Australian Centre for Health & Ageing, Centre for Medical Research, University of Western Australia, Australia; School of Psychiatry & Clinical Neurosciences, University of Western Australia, Australia; Department of Psychiatry, Royal Perth Hospital, Australia.
Abstract
BACKGROUND: Observational studies investigating the association between smoking, cognitive decline and dementia have produced conflicting results. We completed this trial to determine if smoking cessation decreases the progression of cognitive decline in later life.
METHODS: We recruited older smokers (n=229) and never smokers (n=98) and invited smokers to join a smoking cessation trial. The primary outcome of interest was change in Alzheimer’s Disease Assessment Scale cognitive subscale (ADAS-cog) scores over 24months. Secondary measures included the Logical Memory test and changes in gray matter density. Successful smoking cessation was defined as a minimum of 547 smoking free days during follow up.
RESULTS: The ADAS-cog scores of unsuccessful quitters (UQ) increased (i.e., became worse) 1.1±0.3 and 1.2±0.4 points more than the scores of never smokers (NS) (p=0.001) and successful quitters (SQ) (p=0.006) respectively over the 24months of follow up. Similarly, the scores of UQ declined (i.e., became worse) relative to NS on measures of immediate (p=0.004) and delayed recall (p=0.029). All analyses were adjusted for age, years of education, baseline cognitive performance, alcohol use, depression scores, and the presence of chronic respiratory disease. Thirty-six NS, 18 SQ and 48 UQ completed the imaging substudy. Compared with NS, UQ showed a disproportional loss of gray matter density in the right thalamus, right and left inferior semi-lunar lobule, as well as left superior and inferior parietal lobule over 24months. SQ showed loss of gray matter compared with NS in the right middle and inferior occipital gyri, right and left culmen, and the left superior frontal gyrus. We did not find any brain regions in which UQ had lost more gray matter than SQ over 2years.
CONCLUSION: These results are consistent with the hypothesis that smoking causes cognitive decline and loss of gray matter tissue in the brain over time.
Copyright © 2011. Published by Elsevier Inc.
PMID: 21281718 [PubMed - as supplied by publisher]

J Alzheimers Dis. 2011 Feb 1. [Epub ahead of print]

García Y, López-Ramos JC, Giménez-Llort L, Revilla S, Guerra R, Gruart A, Laferla FM, Cristòfol R, Delgado-García JM, Sanfeliu C.
Institute of Biomedical Research of Barcelona (IIBB), CSIC-IDIBAPS, Barcelona, Spain.
Abstract
Physical exercise is considered to exert a positive neurophysiological effect that helps to maintain normal brain activity in the elderly. Expectations that it could help to fight Alzheimer’s disease (AD) were recently raised. This study analyzed the effects of different patterns of physical exercise on the 3xTg-AD mouse. Male and female 3xTg-AD mice at an early pathological stage (4-month-old) have had free access to a running wheel for 1 month, whereas mice at a moderate pathological stage(7-month-old) have had access either during 1 or 6 months. The non-transgenic mouse strain was used as a control. Parallel animal groups were housed in conventional conditions. Cognitive loss and behavioral and psychological symptoms of dementia (BPSD)-like behaviors were present in the 3xTg-AD mice along with alteration in synaptic function and ong-term potentiation impairment in vivo. Brain tissue showed AD-pathology and oxidative-related changes. Disturbances were more severe at the older age tested. Oxidative stress was higher in males but other changes were similar or higher in females. Exercise treatment ameliorated cognitive deterioration and BPSD-like behaviors such as anxiety and the startle response. Synaptic changes were partially protected by exercise. Oxidative stress was reduced. The best neuroprotection was generally obtained after 6 months of exercise in 7-month-old 3xTg-AD mice. Improved sensorimotor function and brain tissue antioxidant defence were induced in both 3xTg-AD and NonTg mice. Therefore, the benefits of aerobic physical exercise on synapse, redox homeostasis, and general brain function demonstrated in the 3xTg-AD mouse further support the value of this healthy life-style against neurodegeneration.
PMID: 21297257 [PubMed - as supplied by publisher]

BACKGROUND/AIMS: An inverse association of educational level with the occurrence of dementia has been repeatedly demonstrated. The mechanism of this relationship is not yet clear. Studies on populations with different educational and occupational levels but uniform living conditions throughout adult life may serve as a natural experiment and may help to rule out lifestyle and environmental factors as possible explanations.

METHODS: We studied the relationship of education, occupational training, and appointment to a leading position with dementia in a cross-sectional study of older female members of a religious order.

RESULTS: Out of 517 eligible sisters, 442 (85.5%) with an average of 54 years membership in the order participated in the study, among which 104 cases of dementia were identified. We found a strong association of low educational and occupational attainment with dementia. The increased risk of dementia was attributable to sisters being poorly educated (age-adjusted OR = 4.5; 95% CI: 2.0-9.9), not having received any vocational training (OR = 9.1; 95% CI: 3.9-20.9), and never having been appointed to a leading position (OR = 3.7; 95% CI: 2.0-7.0).

CONCLUSION: In a setting which largely excludes the influence of lifestyle and environmental factors, we observed a strong association between educational variables and dementia. Our findings support the hypothesis of a reserve capacity against the consequences of brain diseases.

Dement Geriatr Cogn Disord. 2009;27(6):548-56. Epub 2009 Jul 8.

Bickel H, Kurz A.

Department of Psychiatry and Psychotherapy, Technische Universität München, München, Germany. h.bickel@lrz.tum.de

BACKGROUND: Dietary fatty acids and antioxidants may contribute to decrease dementia risk, but epidemiologic data remain controversial. The aim of our study was to analyze the relationship between dietary patterns and risk of dementia or Alzheimer disease (AD), adjusting for sociodemographic and vascular risk factors, and taking into account the ApoE genotype. METHODS: A total of 8,085 nondemented participants aged 65 and over were included in the Three-City cohort study in Bordeaux, Dijon, and Montpellier (France) in 1999-2000 and had at least one re-examination over 4 years (rate of follow-up 89.1%). An independent committee of neurologists validated 281 incident cases of dementia (including 183 AD). RESULTS: Daily consumption of fruits and vegetables was associated with a decreased risk of all cause dementia (hazard ratio [HR] 0.72, 95% CI 0.53 to 0.97) in fully adjusted models. Weekly consumption of fish was associated with a reduced risk of AD (HR 0.65, 95% CI 0.43 to 0.994) and all cause dementia but only among ApoE epsilon 4 noncarriers (HR 0.60, 95% CI 0.40 to 0.90). Regular use of omega-3 rich oils was associated with a decreased risk of borderline significance for all cause dementia (HR 0.46, 95% CI 0.19 to 1.11). Regular consumption of omega-6 rich oils not compensated by consumption of omega-3 rich oils or fish was associated with an increased risk of dementia (HR 2.12, 95% CI 1.30 to 3.46) among ApoE epsilon 4 noncarriers. CONCLUSION: Frequent consumption of fruits and vegetables, fish, and omega-3 rich oils may decrease the risk of dementia and Alzheimer disease, especially among ApoE epsilon 4 noncarriers.

 

1: Neurology. 2007 Nov 13;69(20):1921-30.

Barberger-Gateau P, Raffaitin C, Letenneur L, Berr C, Tzourio C, Dartigues JF, Alpérovitch A.

INSERM, U593, University Victor Segalen Bordeaux 2, case 11, 146 rue Léo-Saignat, F-33076 Bordeaux cedex, France. Pascale.Barberger-Gateau@isped.u-bordeaux2.fr