Alzheimer’s Disease

2017 ◽  
Author(s):  
Michael S. Rafii
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Memory Function ◽  
Hippocampal Atrophy ◽  
Gradual Decline ◽  
Common Cause ◽  
Cognitive Domains ◽  
Prodromal Ad ◽  
Asymptomatic Phase

Alzheimer’s disease (AD) is the most common cause of dementia worldwide, and is characterized by a protracted asymptomatic phase estimated to begin approximately 15 to 20 years. Clinically, AD initially manifests itself by progressive memory impairment, specifically, a loss of episodic memory function characterized by impaired free recall that does not improve with cueing. This is followed by a gradual decline in other cognitive domains leading to functional dependency, which essentially defines the dementia phase of the illness and has been the cornerstone of diagnostic criteria. About 50% of all MCI patients progress to Alzheimer’s dementia, and therefore MCI is thought to represent prodromal AD when they harbor the pathological changes associated with AD, including hippocampal atrophy, elevated CSF amyloid and Tau, as well as the presence of amyloid on PET scan.

scholarly journals Non-Alzheimer's disease-related memory impairment and dementia

2013 ◽  
Vol 15 (4) ◽  
pp. 465-473 ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Clinical Symptoms ◽  
Memory Function ◽  
The Elderly ◽  
Memory Deficits ◽  
Common Cause ◽  
Underlying Causes ◽  
Therapeutic Possibilities

Although Alzheimer's disease (AD) is a common cause of memory impairment and dementia in the elderly disturbed memory function is a widespread subjective and/or objective symptom in a variety of medical conditions. The early detection and correct distinction of AD from non-AD memory impairment is critically important to detect possibly treatable and reversible underlying causes. In the context of clinical research, it is crucial to correctly distinguish between AD or non-AD memory impairment in order to build homogenous study populations for the assessment of new therapeutic possibilities. The distinction of AD from non-AD memory impairment may be difficult, especially in mildly affected patients, due to an overlap of clinical symptoms and biomarker alterations between AD and certain non-AD conditions. This review aims to describe recent aspects of the differential diagnosis of AD and non-AD related memory impairment and how these may be considered in the presence of memory deficits.

Effects of Gossypium herbaceam Extract Administration on the Learning and Memory Function in the Naturally Aged Rats: Neuronal Niche Improvement1

2012 ◽  
Vol 31 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Yanyong Liu ◽  
Haji Akber Aisa ◽  
Chao Ji ◽  
Nan Yang ◽  
Haibo Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Aged Rats

Aging-associated cognitive impairment is an important health care issue since individuals with mild cognitive impairment are more likely to develop Alzheimer’s disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment associated with aging were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70, and 140 mg/kg exerted an improved effect on the learning and memory impairment in aged rats. Subsequently, GHE afforded a beneficial action on eradication of free radicals without influence on the activity of glutathione peroxidase and superoxide dismutase. GHE treatment enhanced the expression levels of nerve growth factor. Meanwhile, proliferation of neural progenitor cells was elevated in hippocampus after treatment with GHE. Taken together, neurogenic niche improvement could be involved in the mechanism underlying neuroprotection of GHE against aging-associated cognitive impairment. These findings suggested that GHE might be a potential agent as cognitive-enhancing drugs that delay or halt mild cognitive impairment progression to Alzheimer’s disease or treatment of aging-associated cognitive impairment.

scholarly journals Deep Learning With 18F-Fluorodeoxyglucose-PET Gives Valid Diagnoses for the Uncertain Cases in Memory Impairment of Alzheimer’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Wei Zhang ◽  
Tianhao Zhang ◽  
Tingting Pan ◽  
Shilun Zhao ◽  
Binbin Nie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Deep Learning ◽  
Mental State ◽  
Fdg Pet ◽  
Neuropsychological Tests ◽  
Memory Impairment ◽  
Memory Function ◽  
Disease Assessment ◽  
18F Fluorodeoxyglucose

Objectives: Neuropsychological tests are an important basis for the memory impairment diagnosis in Alzheimer’s disease (AD). However, multiple memory tests might be conflicting within-subjects and lead to uncertain diagnoses in some cases. This study proposed a framework to diagnose the uncertain cases of memory impairment.Methods: We collected 2,386 samples including AD, mild cognitive impairment (MCI), and cognitive normal (CN) using 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) and three different neuropsychological tests (Mini-Mental State Examination, Alzheimer’s Disease Assessment Scale-Cognitive Subscale, and Clinical Dementia Rating) from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). A deep learning (DL) framework using FDG-PET was proposed to diagnose uncertain memory impairment cases that were conflicting between tests. Subsequent ANOVA, chi-squared, and t-test were used to explain the potential causes of uncertain cases.Results: For certain cases in the testing set, the proposed DL framework outperformed other methods with 95.65% accuracy. For the uncertain cases, its positive diagnoses had a significant (p < 0.001) worse decline in memory function than negative diagnoses in a longitudinal study of 40 months on average. In the memory-impaired group, uncertain cases were mainly explained by an AD metabolism pattern but mild in extent (p < 0.05). In the healthy group, uncertain cases were mainly explained by a non-energetic mental state (p < 0.001) measured using a global deterioration scale (GDS), with a significant depression-related metabolism pattern detected (p < 0.05).Conclusion: A DL framework for diagnosing uncertain cases of memory impairment is proposed. Proved by longitudinal tracing of its diagnoses, it showed clinical validity and had application potential. Its valid diagnoses also provided evidence and explanation of uncertain cases based on the neurodegeneration and depression mental state.

Probable Alzheimer's Disease Patients Presenting as “Focal Temporal Lobe Dysfunction” Show a Slow Rate of Cognitive Decline

2011 ◽  
Vol 18 (1) ◽  
pp. 144-150 ◽  
Author(s):  
Camillo Marra ◽  
Giampiero Villa ◽  
Davide Quaranta ◽  
Alessandro Valenza ◽  
Maria Gabriella Vita ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Semantic Memory ◽  
Temporal Lobe ◽  
Memory Impairment ◽  
Anterograde Amnesia ◽  
Continuous Series ◽  
Cognitive Domains ◽  
Rate Of Progression

AbstractSeveral authors have recently shown that anterograde amnesia is often associated with semantic memory impairment in amnesic MCI patients. Similarly, after the MCI condition, some patients who convert to Alzheimer's disease (AD) show the classic onset (cAD) characterized by the impairment of memory and executive functions, whereas other AD patients show isolated defects of episodic and semantic memory without deficits in other cognitive domains. The latter have been considered an AD variant characterized by ‘focal Temporal Lobe Dysfunction’ (TLD). The aim of the present study was to assess the differences in disease progression between cAD and TLD. For this purpose a continuous series of newly diagnosed probable AD patients presenting as cAD (n = 30) and TLD (n = 25), matched for severity, and 65 healthy controls underwent a comprehensive neuropsychological evaluation at baseline; TLD and cAD were re-evaluated at a 24-month follow-up. At follow-up, TLD patients showed no significant worsening of cognitive functions, whereas cAD subjects displayed a significant worsening in all explored cognitive domains. In conclusion, our results confirm that probable AD presenting as TLD represents a specific onset of AD characterized by a slower rate of progression. (JINS, 2012, 18, 144–150)

Development, Spanish Normative Data, and Validation of a Social Cognition Battery in Prodromal Alzheimer’s Disease and Multiple Sclerosis

2020 ◽  
Author(s):  
Alfonso Delgado-Álvarez ◽  
Vanesa Pytel ◽  
Cristina Delgado-Alonso ◽  
Carmen María Olbrich-Guzmán ◽  
Ana Cortés-Martínez ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Social Cognition ◽  
Neuropsychological Tests ◽  
Normative Data ◽  
Reactivity Index ◽  
Cognitive Domains ◽  
Prodromal Ad ◽  
Prodromal Alzheimer’S Disease

Abstract Objectives The assessment of social cognition changes may be challenging, especially in the earliest stages of some neurodegenerative diseases. Our objective was to validate a social cognition battery from a multidomain perspective. In this regard, we aimed to adapt several tests, collect normative data, and validate them in prodromal Alzheimer’s disease (AD) and multiple sclerosis (MS). Methods A total of 92 healthy controls, 25 prodromal AD, and 39 MS patients were enrolled. Age-, gender-, and education-matched control groups were created for comparisons. Social cognition battery was composed of an emotion-labeling task developed from FACES database, the Story-based Empathy test (SET), the Faux Pas test, and the Interpersonal Reactivity Index. Patients were also evaluated with a comprehensive cognitive battery to evaluate the other cognitive domains. Automatic linear modeling was used to predict each social cognition test’s performance using the neuropsychological tests examining other cognitive domains. Results The reliability of the battery was moderate-high. Significant intergroup differences were found with medium-large effect sizes. Moderate correlations were found between social cognition battery and neuropsychological tests. The emotion labeling task and SET showed moderate correlations with age and education, and age, respectively. Regression-based norms were created considering the relevant demographic variables. Linear regression models including other neuropsychological tests explained between 7.7% and 68.8% of the variance of the social cognition tests performance. Conclusions Our study provides a battery for the assessment of social cognition in prodromal AD and MS with Spanish normative data to improve the evaluation in clinical and research settings.

scholarly journals Evidence for a pervasive autobiographical memory impairment in Logopenic Progressive Aphasia: clinical and neural correlates

2020 ◽  
Author(s):  
Siddharth Ramanan ◽  
David Foxe ◽  
Hashim El-Omar ◽  
Rebekah M. Ahmed ◽  
John R. Hodges ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Autobiographical Memory ◽  
Memory Impairment ◽  
Language Disorder ◽  
Memory Performance ◽  
Memory Function ◽  
Structured Interview ◽  
Progressive Aphasia ◽  
Memory Impairments

ABSTRACTLogopenic Progressive Aphasia is a rare language disorder characterised by repetition and naming difficulties, reflecting the progressive degeneration of left-lateralized peri-sylvian temporal and inferior parietal regions. Mounting evidence suggests that cognitive impairments in this syndrome extend beyond the language domain to include episodic encoding and retrieval disturbances. To date, it remains unknown whether autobiographical memories from across the lifespan are also subject to decline, yet this information is critical to arrive at a comprehensive understanding of the Logopenic syndrome. The objective of this study was to provide the first in depth examination of autobiographical memory function in Logopenic Progressive Aphasia using the Autobiographical Interview, a validated semi-structured interview which assesses recollection of the past under free and probed recall conditions. Autobiographical memory performance in 10 well-characterised Logopenic Progressive Aphasia patients was contrasted with that of 18 typical amnestic Alzheimer’s disease and 16 healthy Control participants. Relative to Controls, Logopenic Progressive Aphasia cases showed marked impairment in the free recall of episodic details, scoring comparably to disease-matched cases of Alzheimer’s disease. This impairment was evident across all time periods and persisted even when formal structured probing was provided. Importantly, controlling for overall level of language disruption failed to ameliorate the autobiographical memory impairment in the Logopenic Progressive Aphasia group, suggesting a genuine amnesia spanning recent and remote memories. Whole-brain voxel-based morphometry analyses revealed that total episodic information retrieved in Logopenic Progressive Aphasia was associated with decreased grey matter intensity predominantly in a bilateral posterior parietal network. Taken together, our findings reveal for the first time the presence of marked remote and recent autobiographical memory impairments in Logopenic Progressive Aphasia, that cannot be explained solely due to their language difficulties or disease staging. Our findings hold important clinical implications for the accurate characterization of Logopenic Progressive Aphasia, and suggest that episodic memory difficulties should be considered as one of the core clinical features of this syndrome.

Mnemonics Usage and Cognitive Decline in Age-Associated Memory Impairment

1997 ◽  
Vol 9 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Gary W. Small ◽  
Asenath La Rue ◽  
Scott Komo ◽  
Andrea Kaplan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Family History ◽  
Cognitive Decline ◽  
Memory Impairment ◽  
Memory Function ◽  
Subjective Memory ◽  
Memory Measure ◽  
History Of

To determine predictors of cognitive deterioration, the authors performed baseline and 1- to 5-year follow-up (mean ± SD = 2.5 ± 1.2 years) neuropsychological assessments on 36 persons (mean age ± SD = 62.1 ± 8.0; range = 50 to 81 years) with age-associated memory impairment. Subjects were recruited from a larger group of volunteers, had minimal medical comorbidity, and 25 of them had a family history of Alzheimer's disease. Baseline age and a subjective memory measure indicating reported frequency of mnemonics usage were significant decline predictors. Subjects reporting more frequent mnemonics use at baseline were more likely to show objective cognitive decline at follow-up. Baseline full-scale IQ, educational level, and family history of Alzheimer's disease failed to predict decline. These findings suggest that although age is the strongest decline predictor in some people with age-associated memory impairment, self-perception of memory function may also predict subsequent cognitive loss.

scholarly journals Brain Functional Network in Alzheimer's Disease: Diagnostic Markers for Diagnosis and Monitoring

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Guido Rodriguez ◽  
Dario Arnaldi ◽  
Agnese Picco
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Functional Brain Imaging ◽  
Common Type ◽  
Functional Networks ◽  
Cognitive Domains ◽  
Brain Functional Network ◽  
Noninvasive Biomarkers ◽  
The Brain

Alzheimer's disease (AD) is the most common type of dementia that is clinically characterized by the presence of memory impairment and later by impairment in other cognitive domains. The clinical diagnosis is based on interviews with the patient and his/her relatives and on neuropsychological assessment, which are also used to monitor cognitive decline over time. Several biomarkers have been proposed for detecting AD in its earliest stages, that is, in the predementia stage. In an attempt to find noninvasive biomarkers, researchers have investigated the feasibility of neuroimaging tools, such as MR, SPECT, and FDG-PET imaging, as well as neurophysiological measurements using EEG. In this paper, we investigate the brain functional networks in AD, focusing on main neurophysiological techniques, integrating with most relevant functional brain imaging findings.

scholarly journals Genetic Interaction of APOE and FGF1 is Associated with Memory Impairment and Hippocampal Atrophy in Alzheimer’s Disease

2019 ◽  
Vol 10 (3) ◽  
pp. 510 ◽  
Author(s):  
Ya-Ting Chang ◽  
Hiroaki Kazui ◽  
Manabu Ikeda ◽  
Chi-Wei Huang ◽  
Shu-Hua Huang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Genetic Interaction ◽  
Hippocampal Atrophy ◽  
With Memory

scholarly journals Natural Medicines and Their Underlying Mechanisms of Prevention and Recovery from Amyloid Β-Induced Axonal Degeneration in Alzheimer’s Disease

2020 ◽  
Vol 21 (13) ◽  
pp. 4665
Author(s):  
Tomoharu Kuboyama ◽  
Ximeng Yang ◽  
Chihiro Tohda
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Network ◽  
Memory Impairment ◽  
Axonal Degeneration ◽  
Memory Function ◽  
Amyloid Β ◽  
In Vivo Models ◽  
Network Disruption ◽  
Ad Therapy

In Alzheimer’s disease (AD), amyloid β (Aβ) induces axonal degeneration, neuronal network disruption, and memory impairment. Although many candidate drugs to reduce Aβ have been clinically investigated, they failed to recover the memory function in AD patients. Reportedly, Aβ deposition occurred before the onset of AD. Once neuronal networks were disrupted by Aβ, they could hardly be recovered. Therefore, we speculated that only removal of Aβ was not enough for AD therapy, and prevention and recovery from neuronal network disruption were also needed. This review describes the challenges related to the condition of axons for AD therapy. We established novel in vitro models of Aβ-induced axonal degeneration. Using these models, we found that several traditional medicines and their constituents prevented or helped recover from Aβ-induced axonal degeneration. These drugs also prevented or helped recover from memory impairment in in vivo models of AD. One of these drugs ameliorated memory decline in AD patients in a clinical study. These results indicate that prevention and recovery from axonal degeneration are possible strategies for AD therapy.

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