The Influence of Co-Morbidity and Frailty on the Clinical Manifestation of Patients with Alzheimer's Disease

2014 ◽  
Vol 42 (2) ◽  
pp. 501-509 ◽  
Author(s):  
Saskia M. Oosterveld ◽  
Roy P.C. Kessels ◽  
Renske Hamel ◽  
Inez H.G.B. Ramakers ◽  
Pauline Aalten ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Manifestation ◽  
Co Morbidity

scholarly journals Case of early-onset Alzheimer’s disease with atypical manifestation

2021 ◽  
Vol 34 (1) ◽  
pp. e100283
Author(s):  
Lin Zhu ◽  
Limin Sun ◽  
Lin Sun ◽  
Shifu Xiao
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Manifestation ◽  
Early Onset ◽  
Short Term Memory ◽  
Brain Mri ◽  
Memory Loss ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Fluent Aphasia

Short-term memory decline is the typical clinical manifestation of Alzheimer’s disease (AD). However, early-onset AD usually has atypical symptoms and may get misdiagnosed. In the present case study, we reported a patient who experienced symptoms of memory loss with progressive non-fluent aphasia accompanied by gradual social withdrawal. He did not meet the diagnostic criteria of AD based on the clinical manifestation and brain MRI. However, his cerebrospinal fluid examination showed a decreased level of beta-amyloid 42, and increased total tau and phosphorylated tau. Massive amyloid β-protein deposition by 11C-Pittsburgh positron emission tomography confirmed the diagnosis of frontal variant AD. This case indicated that early-onset AD may have progressive non-fluent aphasia as the core manifestation. The combination of individual and precision diagnosis would be beneficial for similar cases.

scholarly journals Subjective cognitive decline: The first clinical manifestation of Alzheimer's disease?

2016 ◽  
Vol 10 (3) ◽  
pp. 170-177 ◽  
Author(s):  
Adalberto Studart Neto ◽  
Ricardo Nitrini
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Clinical Manifestation ◽  
Neurodegenerative Disorder ◽  
Subjective Cognitive Decline ◽  
Subjective Memory ◽  
Increased Risk

ABSTRACT Background: Mild cognitive impairment is considered as the first clinical manifestation of Alzheimer's disease (AD), when the individual exhibits below performance on standardized neuropsychological tests. However, some subjects before having a lower performance on cognitive assessments already have a subjective memory complaint. Objective: A review about subjective cognitive decline, the association with AD biomarkers and risk of conversion to dementia. Methods: We performed a comprehensive non-systematic review on PubMed. The keywords used in the search were terms related to subjective cognitive decline. Results: Subjective cognitive decline is characterized by self-experience of deterioration in cognitive performance not detected objectively through formal neuropsychological testing. However, various terms and definitions have been used in the literature and the lack of a widely accepted concept hampers comparison of studies. Epidemiological data have shown that individuals with subjective cognitive decline are at increased risk of progression to AD dementia. In addition, there is evidence that this group has a higher prevalence of positive biomarkers for amyloidosis and neurodegeneration. However, Alzheimer's disease is not the only cause of subjective cognitive decline and various other conditions can be associated with subjective memory complaints, such as psychiatric disorders or normal aging. The features suggestive of a neurodegenerative disorder are: onset of decline within the last five years, age at onset above 60 years, associated concerns about decline and confirmation by an informant. Conclusion: These findings support the idea that subjective cognitive complaints may be an early clinical marker that precedes mild cognitive impairment due to Alzheimer's disease.

Abstract TP433: Subcortical Stroke in E4FAD Transgenic Mice Modulates Amyloid Plaque Accumulation, Motor Recovery After Stroke, and Memory Dysfunction

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Julia Huang ◽  
Edmond Teng ◽  
Gregory Cole ◽  
Jason Hinman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Transgenic Mice ◽  
Motor Recovery ◽  
Mixed Dementia ◽  
Ischemic Lesion ◽  
Co Morbidity ◽  
Pet Ct ◽  
Stroke Group

Introduction: Cerebral microvascular disease and Alzheimer’s disease (AD) account for the majority of dementia diagnoses with 50% of patients having mixed dementia with features of both microvascular stroke in the white matter and AD pathology. This significant co-morbidity indicates an interactive neurobiologic relationship yet it is unclear if these two pathologies synergize or simply co-exist. Methods: To determine the synergistic effect of subcortical stroke on amyloid deposition, focal subcortical white matter ischemic lesion underneath left sensorimotor cortex or sham procedures were introduced at 2 months of age into E4FAD transgenic mice that express the human ApoE4 knock-in allele together with the 5xFAD transgene or littermate controls. Animals underwent behavioral assessment, brain metabolism analysis by PET/CT, and histologic tissue analysis. Results: In E4FAD-positive mice, subcortical stroke vs. sham resulted in a greater inter-hemispheric difference in amyloid burden in the ipsilateral hemisphere (-0.291 vs. -0.078, p=0.08). This was associated with improved motor recovery on rotarod testing in the E4FAD-positive plus stroke group compared to E4FAD-negative stroke group (53.8 sec vs. 45.23 sec, p=0.016). In E4FAD-positive mice, subcortical stroke vs. sham also resulted in improved hippocampal memory function on fear conditioning (17.6+/-5.0 vs. 32.9+/-5.0, p=0.082) while hippocampal plaque number was not significantly different in this cohort. 18 F-FDG PET/CT imaging demonstrated reduced frontal cortex metabolism in the mixed dementia cohort. Conclusions: This novel mouse model of mixed subcortical stroke and Alzheimer’s disease in E4FAD mice illustrates the value of studying the overlap between vascular and Alzheimer’s pathology in the biology of these two common disorders. The combined pathologies demonstrate a potentially paradoxical enhancement in motor recovery and memory impairment compared to stroke or Alzheimer’s disease alone, suggesting that activation of unique molecular pathways in each pathology may partially temper the natural course of each disorder.

scholarly journals Impact of White Matter Changes on Clinical Manifestation of Alzheimer’s Disease

Stroke ◽  
2000 ◽  
Vol 31 (9) ◽  
pp. 2182-2188 ◽  
Author(s):  
Nobutsugu Hirono ◽  
Hajime Kitagaki ◽  
Hiroaki Kazui ◽  
Mamoru Hashimoto ◽  
Etsuro Mori
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Clinical Manifestation ◽  
White Matter Changes

scholarly journals Altered Levels of Neurotrophic Factors in Alzheimer's Disease Patients with a Lifetimne History of Depression

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
M.A. Rapp ◽  
V. Haroutunian ◽  
A. Heinz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Major Depression ◽  
Neurotrophic Factors ◽  
Major Depressive ◽  
Neurotrophin 3 ◽  
Co Morbidity ◽  
History Of ◽  
Underlying Mechanisms ◽  
History Of Depression

Aims:We have recently shown both increases in the number of neuropathological changes in Alzheimer's disease patients with a history of recurrent major depression, and evidence for Alzheimer's disease-related neuropathological changes in patients with geriatric major depression. However, the correlates and possible underlying mechanisms for these neuropathological changes in Alzheimer's disease patients as a function of depression remains to be studied.Method:Levels of several neurotrophic factors, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) were measured in a sample of Alzheimer's disease patients with and without a lifetime history of major depressive disorder.Results:Alzheimer's disease patients with co-morbid depression showed lower levels BDNF (P < .001) and NGF (P < .001) than Alzheimer's disease patients without co-morbid depression. Results remained stable when controlling for age, gender, level of education, and other medical co-morbidities.Conclusion:In Alzheimer's disease, the presence of depression co-morbidity corresponds to decreases in neurotrophic factors beyond effects of age, education, and medical co-morbidities, suggesting that the previously described link between major depression and the neuropathological processes in Alzheimer's disease may be related to changes in neuronal survival mediated by neurotrophic factors.Funded by the National Institute on Aging (U01 AG016976 and NIA P01-AG05138) and NARSAD.

scholarly journals Targeted Nanotherapy for Cognitive Impairment:  Blocking Amyloid-β-Induced Membrane Damage in Brain Tissue

2018 ◽  
Author(s):  
Joseph D'Arrigo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Subjects ◽  
Membrane Damage ◽  
Cell Types ◽  
Cubic Phase ◽  
Type I ◽  
Co Morbidity ◽  
Cns Penetration

A frequent co-morbidity of cerebrovascular pathology and Alzheimer's disease pathology has been observed over past decades. Accordingly, much evidence has been reported which indicates that microvascular endothelial dysfunction, due to cerebrovascular risk factors (e.g., atherosclerosis, obesity, diabetes, smoking, hypertension, aging), precedes cognitive decline in Alzheimer's disease and contributes to its pathogenesis. By incorporating appropriate drug(s) into biomimetic (lipid cubic phase) nanocarriers, one obtains a multitasking combination therapeutic which targets certain cell-surface scavenger receptors, mainly class B type I (i.e., SR-BI), and crosses the blood-brain barrier (BBB). Such targeting allows for various Alzheimer's-related cell types to be simultaneously searched out, in vivo, for localized drug treatment. This in vivo targeting advantage may be particularly important for repurposing an FDA-approved drug, especially one which has shown the added ability to restore some cognitive functions in certain animal models of Alzheimer's disease (e.g., the anticancer drug bexarotene); this (candidate repurposing) drug up to now, by itself (i.e, without nanocarrier), displayed poor CNS penetration in human subjects.

scholarly journals Repair of Oxidative DNA Damage, Cell-Cycle Regulation and Neuronal Death May Influence the Clinical Manifestation of Alzheimer’s Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e99897 ◽  
Author(s):  
Aderbal R. T. Silva ◽  
Ana Cecília Feio Santos ◽  
Jose M. Farfel ◽  
Lea T. Grinberg ◽  
Renata E. L. Ferretti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Dna Damage ◽  
Clinical Manifestation ◽  
Neuronal Death ◽  
Cell Cycle Regulation ◽  
Oxidative Dna Damage ◽  
Damage Cell ◽  
Cycle Regulation

Bilingualism delays clinical manifestation of Alzheimer's disease

2014 ◽  
Vol 18 (3) ◽  
pp. 568-574 ◽  
Author(s):  
EVY WOUMANS ◽  
PATRICK SANTENS ◽  
ANNE SIEBEN ◽  
JAN VERSIJPT ◽  
MICHAËL STEVENS ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Manifestation ◽  
Cognitive Reserve ◽  
Significant Delay ◽  
University Hospitals

The current study investigated the effects of bilingualism on the clinical manifestation of Alzheimer's disease (AD) in a European sample of patients. We assessed all incoming AD patients in two university hospitals within a specified timeframe. Sixty-nine monolinguals and 65 bilinguals diagnosed with probable AD were compared for time of clinical AD manifestation and diagnosis. The influence of other potentially interacting variables was also examined. Results indicated a significant delay for bilinguals of 4.6 years in manifestation and 4.8 years in diagnosis. Our study therefore strengthens the claim that bilingualism contributes to cognitive reserve and postpones the symptoms of dementia.

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