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Article ; Online: Reducing Your Risk of Alzheimer's Dementia: Building a Better Brain as We Age.

Bennett, David A

Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists

2021 Volume 36, Issue 7, Page(s) 1257–1265

Abstract: Alzheimer' dementia is a large and growing public health problem. Of utmost importance for limiting the impact of the disease on society is the prevention of dementia, that is, delay onset either by years whereby death ensues prior to dementia onset. The ...

Abstract	Alzheimer' dementia is a large and growing public health problem. Of utmost importance for limiting the impact of the disease on society is the prevention of dementia, that is, delay onset either by years whereby death ensues prior to dementia onset. The Religious Orders Study and the Rush Memory and Aging Project are two harmonized cohort studies of aging and dementia that include organ donation at death. Ongoing since 1994 and 1997, respectively, we published on the association of numerous experiential, psychological, and medical risk factors for dementia, many of which are potentially modifiable. Here, selected findings are reviewed based on a presentation at the 2020 National Academy of Neuropsychology given virtually in Chicago in October of 2020.
MeSH term(s)	Aging ; Alzheimer Disease/prevention & control ; Brain ; Cohort Studies ; Humans ; Neuropsychological Tests
Language	English
Publishing date	2021-10-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	632972-x
ISSN	1873-5843 ; 0887-6177
ISSN (online)	1873-5843
ISSN	0887-6177
DOI	10.1093/arclin/acab052
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Article ; Online: Author Response: Estrogen Receptor Genes, Cognitive Decline, and Alzheimer Disease.

Oveisgharan, Shahram / Bennett, David A

Neurology

2023 Volume 101, Issue 14, Page(s) 634

MeSH term(s)	Humans ; Female ; Alzheimer Disease/genetics ; Alzheimer Disease/drug therapy ; Receptors, Estrogen/genetics ; Receptors, Estrogen/therapeutic use ; Cognitive Dysfunction/genetics ; Aging ; Estrogen Replacement Therapy
Chemical Substances	Receptors, Estrogen
Language	English
Publishing date	2023-09-28
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000207842
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Article: From theory to practice: translating the concept of cognitive resilience to novel therapeutic targets that maintain cognition in aging adults.

Zammit, Andrea R / Bennett, David A / Buchman, Aron S

Frontiers in aging neuroscience

2024 Volume 15, Page(s) 1303912

Abstract: While the concept of cognitive resilience is well-established it has not been defined in a way that can be measured. This has been an impediment to studying its underlying biology and to developing instruments for its clinical assessment. This ... ...

Abstract	While the concept of cognitive resilience is well-established it has not been defined in a way that can be measured. This has been an impediment to studying its underlying biology and to developing instruments for its clinical assessment. This perspective highlights recent work that has quantified the expression of cortical proteins associated with cognitive resilience, thus facilitating studies of its complex underlying biology and the full range of its clinical effects in aging adults. These initial studies provide empirical support for the conceptualization of resilience as a continuum. Like other conventional risk factors, some individuals manifest higher-than-average cognitive resilience and other individuals manifest lower-than-average cognitive resilience. These novel approaches for advancing studies of cognitive resilience can be generalized to other aging phenotypes and can set the stage for the development of clinical tools that might have the potential to measure other mechanisms of resilience in aging adults. These advances also have the potential to catalyze a complementary therapeutic approach that focuses on augmenting resilience via lifestyle changes or therapies targeting its underlying molecular mechanisms to maintain cognition and brain health even in the presence of untreatable stressors like brain pathologies that accumulate in aging adults.
Language	English
Publishing date	2024-01-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1303912
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Article: Mixed Neuropathologies, Neural Motor Resilience and Target Discovery for Therapies of Late-Life Motor Impairment.

Buchman, Aron S / Bennett, David A

Frontiers in human neuroscience

2022 Volume 16, Page(s) 853330

Abstract: By age 85, most adults manifest some degree of motor impairment. However, in most individuals a specific etiology for motor decline and treatment to modify its inexorable progression cannot be identified. Recent clinical-pathologic studies provide ... ...

Abstract	By age 85, most adults manifest some degree of motor impairment. However, in most individuals a specific etiology for motor decline and treatment to modify its inexorable progression cannot be identified. Recent clinical-pathologic studies provide evidence that mixed-brain pathologies are commonly associated with late-life motor impairment. Yet, while nearly all older adults show some degree of accumulation of Alzheimer's disease and related dementias (ADRD) pathologies, the extent to which these pathologies contribute to motor decline varies widely from person to person. Slower or faster than expected motor decline in the presence of brain injury and/or pathology has been conceptualized as more or less "resilience" relative to the average person This suggests that other factors, such as lifestyles or other neurobiologic indices may offset or exacerbate the negative effects of pathologies
Language	English
Publishing date	2022-03-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2425477-0
ISSN	1662-5161
ISSN	1662-5161
DOI	10.3389/fnhum.2022.853330
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Article ; Online: Single-nucleus RNA velocity reveals critical synaptic and cell-cycle dysregulations in neuropathologically confirmed Alzheimer's disease.

Adewale, Quadri / Khan, Ahmed F / Bennett, David A / Iturria-Medina, Yasser

Scientific reports

2024 Volume 14, Issue 1, Page(s) 7269

Abstract: Typical differential single-nucleus gene expression (snRNA-seq) analyses in Alzheimer's disease (AD) provide fixed snapshots of cellular alterations, making the accurate detection of temporal cell changes challenging. To characterize the dynamic cellular ...

Abstract	Typical differential single-nucleus gene expression (snRNA-seq) analyses in Alzheimer's disease (AD) provide fixed snapshots of cellular alterations, making the accurate detection of temporal cell changes challenging. To characterize the dynamic cellular and transcriptomic differences in AD neuropathology, we apply the novel concept of RNA velocity to the study of single-nucleus RNA from the cortex of 60 subjects with varied levels of AD pathology. RNA velocity captures the rate of change of gene expression by comparing intronic and exonic sequence counts. We performed differential analyses to find the significant genes driving both cell type-specific RNA velocity and expression differences in AD, extensively compared these two transcriptomic metrics, and clarified their associations with multiple neuropathologic traits. The results were cross-validated in an independent dataset. Comparison of AD pathology-associated RNA velocity with parallel gene expression differences reveals sets of genes and molecular pathways that underlie the dynamic and static regimes of cell type-specific dysregulations underlying the disease. Differential RNA velocity and its linked progressive neuropathology point to significant dysregulations in synaptic organization and cell development across cell types. Notably, most of the genes underlying this synaptic dysregulation showed increased RNA velocity in AD subjects compared to controls. Accelerated cell changes were also observed in the AD subjects, suggesting that the precocious depletion of precursor cell pools might be associated with neurodegeneration. Overall, this study uncovers active molecular drivers of the spatiotemporal alterations in AD and offers novel insights towards gene- and cell-centric therapeutic strategies accounting for dynamic cell perturbations and synaptic disruptions.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; RNA/genetics ; Transcriptome/genetics ; Gene Expression Profiling ; Solitary Nucleus/metabolism
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2024-03-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-57918-x
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Article ; Online: Lack of Benefit With Idalopirdine for Alzheimer Disease: Another Therapeutic Failure in a Complex Disease Process.

Bennett, David A

JAMA

2018 Volume 319, Issue 2, Page(s) 123–125

MeSH term(s)	Alzheimer Disease ; Humans
Language	English
Publishing date	2018-01-08
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2958-0
ISSN	1538-3598 ; 0254-9077 ; 0002-9955 ; 0098-7484
ISSN (online)	1538-3598
ISSN	0254-9077 ; 0002-9955 ; 0098-7484
DOI	10.1001/jama.2017.19700
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Article ; Online: An MRI biomarker of mixed pathology.

Bennett, David A

Neurology

2018 Volume 91, Issue 15, Page(s) 682–683

MeSH term(s)	Alzheimer Disease ; Biomarkers ; Humans ; Magnetic Resonance Imaging
Chemical Substances	Biomarkers
Language	English
Publishing date	2018-09-14
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000006305
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Article ; Online: Aducanumab and the "post-amyloid" era of Alzheimer research?

Musiek, Erik S / Bennett, David A

Neuron

2021 Volume 109, Issue 19, Page(s) 3045–3047

MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/drug therapy ; Amyloid ; Antibodies, Monoclonal, Humanized/therapeutic use ; Device Approval ; History, 19th Century ; History, 20th Century ; Humans ; Immunotherapy ; Middle Aged ; Plaque, Amyloid
Chemical Substances	Amyloid ; Antibodies, Monoclonal, Humanized ; aducanumab (105J35OE21)
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Historical Article ; Journal Article
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2021.09.007
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Article ; Online: Lower GLUT1 and unchanged MCT1 in Alzheimer's disease cerebrovasculature.

Leclerc, Manon / Tremblay, Cyntia / Bourassa, Philippe / Schneider, Julie A / Bennett, David A / Calon, Frédéric

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2024 , Page(s) 271678X241237484

Abstract: The brain is a highly demanding organ, utilizing mainly glucose but also ketone bodies as sources of energy. Glucose transporter-1 (GLUT1) and monocarboxylates transporter-1 (MCT1) respectively transport glucose and ketone bodies across the blood-brain ... ...

Abstract	The brain is a highly demanding organ, utilizing mainly glucose but also ketone bodies as sources of energy. Glucose transporter-1 (GLUT1) and monocarboxylates transporter-1 (MCT1) respectively transport glucose and ketone bodies across the blood-brain barrier. While reduced glucose uptake by the brain is one of the earliest signs of Alzheimer's disease (AD), no change in the uptake of ketone bodies has been evidenced yet. To probe for changes in GLUT1 and MCT1, we performed Western immunoblotting in microvessel extracts from the parietal cortex of 60 participants of the Religious Orders Study. Participants clinically diagnosed with AD had lower cerebrovascular levels of GLUT1, whereas MCT1 remained unchanged. GLUT1 reduction was associated with lower cognitive scores. No such association was found for MCT1. GLUT1 was inversely correlated with neuritic plaques and cerebrovascular β-secretase-derived fragment levels. No other significant associations were found between both transporters, markers of Aβ and tau pathologies, sex, age at death or apolipoprotein-ε4 genotype. These results suggest that, while a deficit of GLUT1 may underlie the reduced transport of glucose to the brain in AD, no such impairment occurs for MCT1. This study thus supports the exploration of ketone bodies as an alternative energy source for the aging brain.
Language	English
Publishing date	2024-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X241237484
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Article ; Online: The time course of motor and cognitive decline in older adults and their associations with brain pathologies: a multicohort study.

Oveisgharan, Shahram / Wang, Tianhao / Barnes, Lisa L / Schneider, Julie A / Bennett, David A / Buchman, Aron S

The lancet. Healthy longevity

2024

Abstract: Background: Many studies have reported that impaired gait precedes cognitive impairment in older people. We aimed to characterise the time course of cognitive and motor decline in older individuals and the association of these declines with the ... ...

Abstract	Background: Many studies have reported that impaired gait precedes cognitive impairment in older people. We aimed to characterise the time course of cognitive and motor decline in older individuals and the association of these declines with the pathologies of Alzheimer's disease and related dementias. Methods: This multicohort study used data from three community-based cohort studies (Religious Orders Study, Rush Memory and Aging Project, and Minority Aging Research Study, all in the USA). The inclusion criteria for all three cohorts were no clinical dementia at the time of enrolment and consent to annual clinical assessments. Eligible participants consented to post-mortem brain donation and had post-mortem pathological assessments and three or more repeated annual measures of cognition and motor functions. Clinical and post-mortem data were analysed using functional mixed-effects models. Global cognition was based on 19 neuropsychological tests, a hand strength score was based on grip and pinch strength, and a gait score was based on the number of steps and time to walk 8 feet and turn 360°. Brain pathologies of Alzheimer's disease and related dementias were assessed at autopsy. Findings: From 1994 to 2022, there were 1570 eligible cohort participants aged 65 years or older, 1303 of whom had cognitive and motor measurements and were included in the analysis. Mean age at death was 90·3 years (SD 6·3), 905 (69%) participants were female, and 398 (31%) were male. Median follow-up time was 9 years (IQR 5-11). On average, cognition was stable from 25 to 15 years before death, when cognition began to decline. By contrast, gait function and hand strength declined during the entire study. The combinations of pathologies of Alzheimer's disease and related dementias associated with cognitive and motor decline and their onsets of associations varied; only tau tangles, Parkinson's disease pathology, and macroinfarcts were associated with decline of all three phenotypes. Tau tangles were significantly associated with cognitive decline, gait function decline, and hand function decline (p<0·0001 for each); however, the association with cognitive decline persisted for more than 11 years before death, but the association with hand strength only began 3·57 years before death and the association with gait began 3·49 years before death. By contrast, the association of macroinfarcts with declining gait function began 9·25 years before death (p<0·0001) compared with 6·65 years before death (p=0·0005) for cognitive decline and 2·66 years before death (p=0·024) for decline in hand strength. Interpretation: Our findings suggest that average motor decline in older adults precedes cognitive decline. Macroinfarcts but not tau tangles are associated with declining gait function that precedes cognitive decline. This suggests the need for further studies to test if gait impairment is a clinical proxy for preclinical vascular cognitive impairment. Funding: National Institutes of Health.
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ISSN	2666-7568
ISSN (online)	2666-7568
DOI	10.1016/S2666-7568(24)00033-3
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