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Background In preclinical Alzheimer’s disease, it is unclear why some individuals with amyloid pathologic change are asymptomatic (stage 1), whereas others experience subjective cognitive decline (SCD, stage 2). Here, we examined the association of stage 1 vs. stage 2 with structural brain reserve in memory-related brain regions. Methods We tested whether the volumes of hippocampal subfields and parahippocampal regions were larger in individuals at stage 1 compared to asymptomatic amyloid-negative older adults (healthy controls, HCs). We also tested whether individuals with stage 2 would show the opposite pattern, namely smaller brain volumes than in amyloid-negative individuals with SCD. Participants with cerebrospinal fluid (CSF) biomarker data and bilateral volumetric MRI data from the observational, multi-centric DZNE-Longitudinal Cognitive Impairment and Dementia Study (DELCODE) study were included. The sample comprised 95 amyloid-negative and 26 amyloid-positive asymptomatic participants as well as 104 amyloid-negative and 47 amyloid-positive individuals with SCD. Volumes were based on high-resolution T2-weighted images and automatic segmentation with manual correction according to a recently established high-resolution segmentation protocol. Results In asymptomatic individuals, brain volumes of hippocampal subfields and of the parahippocampal cortex were numerically larger in stage 1 compared to HCs, whereas the opposite was the case in individuals with SCD. MANOVAs with volumes as dependent data and age, sex, years of education, and DELCODE site as covariates showed a significant interaction between diagnosis (asymptomatic versus SCD) and amyloid status (Aß42/40 negative versus positive) for hippocampal subfields. Post hoc paired comparisons taking into account the same covariates showed that dentate gyrus and CA1 volumes in SCD were significantly smaller in amyloid-positive than negative individuals. In contrast, CA1 volumes were significantly ( p  = 0.014) larger in stage 1 compared with HCs. Conclusions These data indicate that HCs and stages 1 and 2 do not correspond to linear brain volume reduction. Instead, stage 1 is associated with larger than expected volumes of hippocampal subfields in the face of amyloid pathology. This indicates a brain reserve mechanism in stage 1 that enables individuals with amyloid pathologic change to be cognitively normal and asymptomatic without subjective cognitive decline.

INTRODUCTION This review examines the concept of cognitive reserve (CR) in relation to brain aging, particularly in the context of dementia and its early stages. CR refers to an individual's ability to maintain or regain cognitive function despite brain aging, damage, or disease. Various factors, including education, occupation complexity, leisure activities, and genetics are believed to influence CR. METHODS We revised the literature in the context of CR. A total of 842 articles were identified, then we rigorously assessed the relevance of articles based on titles and s, employing a systematic approach to eliminate studies that did not align with our research objectives. RESULTS We evaluate—also in a critical way—the methods commonly used to define and measure CR, including sociobehavioral proxies, neuroimaging, and electrophysiological and genetic measures. The challenges and limitations of these measures are discussed, emphasizing the need for more targeted research to improve the understanding, definition, and measurement of CR. CONCLUSIONS The review underscores the significance of comprehending CR in the context of both normal and pathological brain aging and emphasizes the importance of further research to identify and enhance this protective factor for cognitive preservation in both healthy and neurologically impaired older individuals. Highlights This review examines the concept of cognitive reserve in brain aging, in the context of dementia and its early stages. We have evaluated the methods commonly used to define and measure cognitive reserve. Sociobehavioral proxies, neuroimaging, and electrophysiological and genetic measures are discussed. The review emphasizes the importance of further research to identify and enhance this protective factor for cognitive preservation.

Cognitive reserve (CR) prevents cognitive decline and delays neurodegeneration. Recent epidemiological evidence suggests that lifelong bilingualism may act as CR delaying the onset of dementia by ∼4.5 y. Much controversy surrounds the issue of bilingualism and its putative neuroprotective effects. We studied brain metabolism, a direct index of synaptic function and density, and neural connectivity to shed light on the effects of bilingualism in vivo in Alzheimer’s dementia (AD). Eighty-five patients with probable AD and matched for disease duration (45 German-Italian bilingual speakers and 40 monolingual speakers) were included. Notably, bilingual individuals were on average 5 y older than their monolingual peers. In agreement with our predictions and with models of CR, cerebral hypometabolism was more severe in the group of bilingual individuals with AD. The metabolic connectivity analyses crucially supported the neuroprotective effect of bilingualism by showing an increased connectivity in the executive control and the default mode networks in the bilingual, compared with the monolingual, AD patients. Furthermore, the degree of lifelong bilingualism (i.e., high, moderate, or low use) was significantly correlated to functional modulations in crucial neural networks, suggesting both neural reserve and compensatory mechanisms. These findings indicate that lifelong bilingualism acts as a powerful CR proxy in dementia and exerts neuroprotective effects against neurodegeneration. Delaying the onset of dementia is a top priority of modern societies, and the present in vivo neurobiological evidence should stimulate social programs and interventions to support bilingual or multilingual education and the maintenance of the second language among senior citizens.

Resting state brain activity consumes most of brain energy, likely creating and maintaining a reserve of general brain functionality. The latent reserve if it exists may be reflected by the profound long-range fluctuations of resting brain activity. The long-range temporal coherence (LRTC) can be characterized by resting state fMRI (rsfMRI)-based brain entropy (BEN) mapping. While BEN mapping results have shown sensitivity to neuromodulations or disease conditions, the underlying neuromechanisms especially the associations of BEN or LRTC to neurocognition still remain unclear. To address this standing question and to test a novel hypothesis that resting BEN reflects a latent functional reserve through the link to general functionality, we mapped resting BEN of 862 young adults and comprehensively examined its associations to neurocognitions using data from the Human Connectome Project (HCP). Our results unanimously highlighted two brain circuits: the default mode network (DMN) and executive control network (ECN) through their negative associations of BEN to general functionality, which is independent of age and sex. While BEN in DMN/ECN increases with age, it decreases with education years. These results demonstrated the neurocognitive correlates of resting BEN in DMN/ECN and suggest resting BEN in DMN/ECN as a potential proxy of the latent functional reserve that facilitates general brain functionality and may be enhanced by education. [Display omitted]

Background and aims: The concept of “reserve” has been used to explain the difference between individuals in their capacity to cope with or compensate for pathology. Brain reserve refers to structural aspects of the brain, such as brain size and synapse count. Cognitive reserve is the ability to optimize and maximize performance through two mechanisms: recruitment of brain networks, and/or compensation by alternative cognitive strategies. The aim of the present research was to devise an instrument for comprehensive assessment and measurement of the quantity of cognitive reserve accumulated by individuals throughout their lifespan. Methods: A new approach using the Cognitive Reserve Index questionnaire (CRIq) was developed and tested in a sample of 588 healthy individuals, from 18 to 102 years old, stratified by age (Young, Adults, Elderly) and gender. The CRIq includes demographic data and items grouped into three sections: education, working activity and leisure time, each of which returns a subscore. The WAIS Vocabulary test and TIB were also administered. Results: The main descriptive features and some inferential results are described. Intelligence was only moderately correlated with cognitive reserve, stressing the distinction between these two concepts. Age and gender significantly affected CRIq scores, whereas no effect emerged from their interaction. Adults showed a higher score than Young and Elderly. Conclusions: This study provides a new instrument for a standardized measure of the cognitive reserve accumulated by individuals through their lifespan. The potential use of the CRIq in both experimental research and clinical practice is discussed.

Increasing attention has been given to understanding resilience to brain diseases, often described as brain or cognitive reserve. Among the protective factors for the development of resilience, physical activity/exercise has been considered to play an important role. Exercise is known to induce many positive effects on the brain. As such, exercise represents an important tool to influence neurodevelopment and shape the adult brain to react to life's challenges. Among many beneficial effects, exercise intervention has been associated with cognitive improvement and stress resilience in humans and animal models. Thus, a growing number of studies have demonstrated that exercise not only recovers or minimizes cognitive deficits by inducing better neuroplasticity and cognitive reserve but also counteracts brain pathology. This is evidenced before disease onset or after it has been established. In this review, we aimed to present encouraging data from current clinical and pre-clinical neuroscience research and discuss the possible biological mechanisms underlying the beneficial effects of physical exercise on resilience. We consider the implication of physical exercise for resilience from brain development to aging and for some neurological diseases. Overall, the literature indicates that brain/cognitive reserve built up by regular exercise in several stages of life, prepares the brain to be more resilient to cognitive impairment and consequently to brain pathology.

The goal of this paper is to review my current understanding of the concepts of cognitive reserve (CR), brain reserve and brain maintenance, and to describe our group’s approach to using imaging to study their neural basis. I present a working model for utilizing data regarding brain integrity, clinical status, cognitive activation and CR proxies to develop analyses that can explore the neural basis of cognitive reserve and brain maintenance. The basic model assumes that the effect of brain changes on cognition is mediated by task-related activation. We treat CR as a moderator to understand how task-related activation might vary as a function of CR, or how CR might operate independently of these differences in task-related activation. My hope is that this presentation will spark discussion across groups that study these concepts, allowing us to come to some common agreement on definitions, methodology and approaches.

INTRODUCTION Alzheimer's disease (AD) patients with higher educational attainment (EA) often exhibit better cognitive function. However, the relationship among EA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation. METHODS We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA). We examined the effects of Aβ plaques, tau tangles, and gray matter volume (GMV) on the relationship between EA and domain‐specific cognitive decline. RESULTS A+/High‐EA individuals exhibited slower cognitive decline in global cognition and language domains than A+/Low‐EA individuals. This cognitive benefit was independently and synergistically explained by reduced AD pathology, including lower Aβ and tau burdens, as well as preserved GMV. Additionally, High‐EA individuals experienced a median delay of 1.9 years in the onset of significant brain atrophy among A+ individuals. DISCUSSION These findings highlight the independent and synergistic contributions of EA‐associated AD pathology and GMV alterations to longitudinal cognitive decline. Highlights Alzheimer's disease (AD) individuals with high educational attainment (EA) show slower declines in global cognition and language. EA‐related slower cognitive decline is linked to reduced tau and greater gray matter volume in AD. AD individuals with high EA show a median 1.9 year delayed onset of brain atrophy.

Background The concept of reserve was established to account for the observation that a given degree of neurodegenerative pathology may result in varying degrees of symptoms in different individuals. There is a large amount of evidence on epidemiological risk and protective factors for neurodegenerative diseases and dementia, yet the biological mechanisms that underpin the protective effects of certain lifestyle and physiological variables remain poorly understood, limiting the development of more effective preventive and treatment strategies. Additionally, different definitions and concepts of reserve exist, which hampers the coordination of research and comparison of results across studies. Discussion This paper represents the consensus of a multidisciplinary group of experts from different areas of research related to reserve, including clinical, epidemiological and basic sciences. The consensus was developed during meetings of the working groups of the first International Conference on Cognitive Reserve in the Dementias (24–25 November 2017, Munich, Germany) and the Alzheimer’s Association Reserve and Resilience Professional Interest Area (25 July 2018, Chicago, USA). The main objective of the present paper is to develop a translational perspective on putative mechanisms underlying reserve against neurodegenerative disease, combining evidence from epidemiological and clinical studies with knowledge from animal and basic research. The potential brain functional and structural basis of reserve in Alzheimer’s disease and other brain disorders are discussed, as well as relevant lifestyle and genetic factors assessed in both humans and animal models. Conclusion There is an urgent need to advance our concept of reserve from a hypothetical model to a more concrete approach that can be used to improve the development of effective interventions aimed at preventing dementia. Our group recommends agreement on a common dictionary of terms referring to different aspects of reserve, the improvement of opportunities for data sharing across individual cohorts, harmonising research approaches across laboratories and groups to reduce heterogeneity associated with human data, global coordination of clinical trials to more effectively explore whether reducing epidemiological risk factors leads to a reduced burden of neurodegenerative diseases in the population, and an increase in our understanding of the appropriateness of animal models for reserve research.