scholarly journals Neurophysiological and Brain Structural Markers of Cognitive Frailty Differ from Alzheimer’s Disease

2022 ◽  
pp. JN-RM-0697-21
Author(s):  
Ece Kocagoncu ◽  
David Nesbitt ◽  
Tina Emery ◽  
Laura Hughes ◽  
Richard N. Henson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Frailty

scholarly journals Blood-based protein mediators of senility with replications across biofluids and cohorts

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Donald R Royall ◽  
Raymond F Palmer ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Serum Proteins ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Protein Biomarkers ◽  
Cognitive Frailty ◽  
Mediation Effects ◽  
Dementia Severity ◽  
Biology Of Aging

Abstract Dementia severity can be quantitatively described by the latent dementia phenotype ‘δ’ and its various composite ‘homologues’. We have explored δ’s blood-based protein biomarkers in the Texas Alzheimer’s Research and Care Consortium. However, it would be convenient to replicate them in the Alzheimer’s Disease Neuroimaging Initiative. To that end, we have engineered a δ homologue from the observed cognitive performance measures common to both projects [i.e. ‘d:Texas Alzheimer’s Research and Care Consortium to Alzheimer’s Disease Neuroimaging Initiative’ (dT2A)]. In this analysis, we confirm 13/22 serum proteins as partial mediators of age’s effect on dementia severity as measured by dT2A in the Texas Alzheimer’s Research and Care Consortium and then replicate 4/13 in the Alzheimer’s Disease Neuroimaging Initiative’s plasma data. The replicated mediators of age-specific effects on dementia severity are adiponectin, follicle-stimulating hormone, pancreatic polypeptide and resistin. In their aggregate, the 13 confirmed age-specific mediators suggest that ‘cognitive frailty’ pays a role in dementia severity as measured by δ. We provide both discriminant and concordant support for that hypothesis. Weight, calculated low-density lipoprotein and body mass index are partial mediators of age’s effect in the Texas Alzheimer’s Research and Care Consortium. Biomarkers related to other disease processes (e.g. cerebrospinal fluid Alzheimer’s disease-specific biomarkers in the Alzheimer’s Disease Neuroimaging Initiative) are not. It now appears that dementia severity is the sum of multiple independent processes impacting δ. Each may have a unique set of mediating biomarkers. Age’s unique effect appears to be at least partially mediated through proteins related to frailty. Age-specific mediation effects can be replicated across cohorts and biofluids. These proteins may offer targets for the remediation of age-specific cognitive decline (aka ‘senility’), help distinguish it from other determinants of dementia severity and/or provide clues to the biology of Aging Proper.

THE COMPLEX CONSTRUCT OF MILD COGNITIVE IMPAIRMENT: BE AWARE OF COGNITIVE FRAILTY

2014 ◽  
pp. 1-2
Author(s):  
M. CANEVELLI ◽  
E. KELAIDITI
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Sample Size ◽  
Limited Sample ◽  
Validity Of Results ◽  
Cognitive Frailty ◽  
Limited Sample Size ◽  
Specific Relationship

A recent study in the Journal of Frailty & Aging (1)investigated the stage-specific relationship between frailty andcognitive impairment among individuals attending a MemoryClinic. The Authors hypothesized that worsening of cognitivedecline may lead to increased frailty prevalence, beingcognition a well-established contributor to individualvulnerability and resiliency to stressors. Nevertheless,seemingly counter-intuitively, they observed a “U-shaped”relationship between frailty and cognitive impairment. Inparticular, the frailty prevalence was higher among individualsdiagnosed as mild cognitive impairment (MCI), was lower inmild Alzheimer’s disease (AD) patients, and again increased insubjects affected by moderate AD. The study, despite somemethodological issues potentially limiting the validity of results(i.e. the limited sample size), offers the opportunity to discussseveral important aspects.

scholarly journals Alzheimer’s Disease and Cognitive Frailty: Novel Therapeutic Technologies

2016 ◽  
Vol 2016 ◽  
pp. 1-2
Author(s):  
Grazia D’Onofrio ◽  
Zhuowei Yu ◽  
Orestes V. Forlenza
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Frailty ◽  
Novel Therapeutic

scholarly journals Potential fluid biomarkers for pathological brain changes in Alzheimer's disease: Implication for the screening of cognitive frailty

2016 ◽  
Vol 14 (4) ◽  
pp. 3184-3198 ◽  
Author(s):  
Qingwei Ruan ◽  
Grazia D'Onofrio ◽  
Daniele Sancarlo ◽  
Antonio Greco ◽  
Zhuowei Yu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Frailty ◽  
Brain Changes ◽  
Potential Fluid

scholarly journals Neurophysiological and brain structural markers of cognitive frailty differs from Alzheimer’s disease

2021 ◽  
Author(s):  
Ece Kocagoncu ◽  
David Nesbitt ◽  
Tina Emery ◽  
Laura Hughes ◽  
Richard N. Henson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Healthy Aging ◽  
Grey Matter ◽  
Grey Matter Volume ◽  
Cognitive Frailty ◽  
Clinical Presentations ◽  
Normal Ageing

AbstractWith increasing life span, there is growing importance of understanding the mechanisms of successful cognitive ageing. In contrast, cognitive frailty has been proposed to be a precursor to Alzheimer’s disease. Here we test the hypothesis that cognitively frail adults represent a branch of healthy ageing, distinct from latent dementia. We used electro-magnetoencephalography and magnetic resonance imaging to investigate the structural and neurophysiological features of cognitive frailty in relation to healthy aging, and clinical presentations of mild cognitive impairment and Alzheimer’s disease. Cognitive performance of the cognitively frail group was similar to those with mild cognitive impairment. We used a novel cross-modal oddball task to induce mismatch responses to unexpected stimuli. Both controls and cognitively frail showed stronger mismatch responses and larger temporal grey matter volume, compared to people with mild cognitive impairment and Alzheimer’s disease. Our results suggest that cognitively frail represents a spectrum of normal ageing rather than incipient or undiagnosed Alzheimer’s disease. Lower cognitive reserve, hearing impairment and medical comorbidity might contribute to the aetiology of cognitive impairment.

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.

Formation of paired helical filaments in Alzheimer's disease

1984 ◽  
Vol 42 ◽  
pp. 302-303
Author(s):  
J. Metuzals ◽  
D. F. Clapin ◽  
V. Montpetit
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Lobe ◽  
Giant Axon ◽  
Paired Helical Filaments ◽  
Normal Brain ◽  
Protein Assemblies ◽  
Electron Microscopic ◽  
Helical Symmetry ◽  
Structural Levels

Information on the conformation of paired helical filaments (PHF) and the neurofilamentous (NF) network is essential for an understanding of the mechanisms involved in the formation of the primary lesions of Alzheimer's disease (AD): tangles and plaques. The structural and chemical relationships between the NF and the PHF have to be clarified in order to discover the etiological factors of this disease. We are investigating by stereo electron microscopic and biochemical techniques frontal lobe biopsies from patients with AD and squid giant axon preparations. The helical nature of the lesion in AD is related to pathological alterations of basic properties of the nervous system due to the helical symmetry that exists at all hierarchic structural levels in the normal brain. Because of this helical symmetry of NF protein assemblies and PHF, the employment of structure reconstruction techniques to determine the conformation, particularly the handedness of these structures, is most promising. Figs. 1-3 are frontal lobe biopsies.

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