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The concept of subjective cognitive decline (SCD) is currently receiving much attention, as SCD has a high risk of transitioning to mild cognitive impairment (MCI) and dementia. The ATN biomarker diagnostic framework can accurately diagnose SCD as preclinical Alzheimer's disease (AD), which is an important window for precise prevention and treatment of AD. Based on the present diagnostic paradigms of clinical diagnosis and biomarker diagnosis for SCD, it is important to have fine management during the diagnostic process and precise communication and support after diagnosis for SCD patients, including diagnostic management specification, interpretation and recommendation diagnostic of biomarker disclosure, patients health management, and possible treatment for specific underlying causes. Previous studies have shown heterogeneity between clinical research and practice, and many doctors still feel unfamiliar with the concept of SCD and lack a systematic understanding. SCD diagnosis can provide patients with a certain degree of certainty, but it may also bring uncertainty about the expected risk of disease, and there is an urgent need to provide guidance to clinical doctors. So far, there is still a lack of Chinese expert consensus on diagnostic management specification, biomarker disclosure, and patient management of SCD. Based on the systematic summary of the current domestic and international research on the SCD, the consensus is written and aimed to improve the diagnosis and treatment level of SCD, guide high-quality preclinical AD research and lay the foundation for further clinical translation. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common type of dementia in the elderly. The ApoE ε4 gene is the main genetic risk factors for sporadic AD, and is associated with the changes in the amyloid (3- protein (Aβ) and tau protein, the core pathological features of AD. ApoE ε4 has great potential as a genetic biomarker for AD. Clinical studies have shown the important role of peripheral blood ApoE ε4 in AD risk assessment and disease detection. But in the current clinical practice, there are many weak points of insufficient understanding and insufficient attention about the clinical use of ApoE ε4. The importance of ApoE ε4 is highlighted especially with the development of high-quality clinical drug trials or the arrival of clinical drug therapy targeting Aβ for AD. So far, there is still a lack of Chinese expert consensus on the standardized application of ApoE ε4 in AD. Given that, this article systematically summarizes the current domestic and international research on the application of ApoE ε4 in AD. The consensus is written and aimed to fully reflect the clinical application value of ApoE ε4 in AD, and improve the diagnosis and treatment level of AD, and guide further clinical research. [ABSTRACT FROM AUTHOR]

Objective To report clinical phenotype and gene mutation characteristics of one case of early-onset Alzheimer's disease (EOAD) associated with PSEN2 V214L mutation and conduct a pedigree analysis. Methods and Results A 63-year-old male proband with no family history of dementia, onset at 58 years old, had memory loss as the first manifestation and progressive aggravation of symptoms. Neuropsychological tests showed a score of 1 on Mini-Mental State Examination (MMSE), 0 on Montreal Cognitive Assessment (MoCA), 71 on Activities of Daily Living Scale (ADL), and 3 on Hachinski Ischemic Score (HIS). Head MRI revealed extensive cortical atrophy, with prominent atrophy of bilateral hippocampal, multiple hyperintensity in deep white matter (Fazekas grade 2). Exons of high-throughput sequencing of dementia-related genes showed that both the proband and his sister had heterozygous missense mutations in exon 8 of PSEN2 gene c.640G > T (p.V214L) and heterozygous splicing mutations in exon 28 of SORL1 gene c.3815-4A > C. The proband was finally diagnosed with EOAD associated with PSEN2 V214L mutation, and the proband's sister was considered as an absolute risk group for Alzheimer's disease (AD). Conclusions The PSEN2 V214L mutation probably causes EOAD. Further investigations should be conducted to evaluate the effects on the production of amyloid β-protein 40 and 42 (Aβ40 and Aβ42), then verify its pathogenicity. [ABSTRACT FROM AUTHOR]

Subjective cognitive decline (SCD) refers to the preclinical stage of Alzheimer's disease (AD) in which patients have the chief complaint of cognitive decline but no objective manifestations. It is considered to be an earlier stage of mild cognitive impairment (MCI) than the preclinical stage of AD, and the risk of progression to AD is higher. At present, there is a limited understanding of SCD in China. This paper reviews the concept of SCD, the status quo of epidemiological research, research framework, related risk factors, its relationship with AD, as well as the progress of neuropsychological tests and imaging research, so as to provide the possibility for the early clinical diagnosis and treatment of AD. [ABSTRACT FROM AUTHOR]

Neurodegenerative diseases are a group of disorders in which progressive loss of neurons due to abnormal protein deposits causes structural and functional changes in the brain, including Alzheimer's disease (AD), Parkinson's disease (PD), dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). In brain imaging studies of neurodegenerative diseases, resting-state fMRI (rs-fMRI) has been widely used, with most studies analysing static features of brain function. However, the human brain is dynamic and its neural activity is non - stationary, and static studies can not reveal the time - varying features of brain function. In recent years, many studies have used dynamic analysis of brain function based on rs-fMRI in order to reveal the dynamic nature of complex neural activity in the brain and further investigate the pathophysiological mechanisms and diagnostic markers of disease. In this paper, we will briefly introduce the rs-fMRI analysis method, the common methods of rs-fMRI-based dynamic analysis of brain function and its application and research progress in common neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

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Background To summarize the clinical, genotype and olfactory characteristic in patients with 11C-Pittsburgh compound B (11C-PIB)-positive cognitive impairment. Methods Twenty-seven patients with 11C-PIB-positive cognitive impairment, including 19 patients with Alzheimer's disease (AD) and 8 patients with mild cognitive impairment (MCI), were recruited from January 2015 to February 2016 in Tianjin Huanhu Hospital. The clinical, genotype and olfactory profiles were retrospectively analyzed. Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and Clock Drawing Test (CDT), Neuropsychiatric Inventory (NPI), Activity of Daily Living Scale (ADL), and Hamilton Depression Scale-21 (HAMD-21) were used to evaluate cognitive function, behavioral and psychological symptoms, activities of daily living, and symptoms of depression, respectively. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to determine ApoE genotype, and T&T olfactometer was used to test threshold of detection and recognition. Results Compared with MCI patients, AD patients had lower MMSE score (P = 0.000), orientation to time (P = 0.031), short-term memory (P = 0.021), recall (P = 0.009), calculation (P = 0.000), repetition (P = 0.038), reading (P = 0.021), writing (P = 0.002), visual-spatial ability (P = 0.039), MoCA score (P = 0.000) and CDT score (P = 0.020), and higher ADL score (P = 0.000). But there was no significant difference in orientation to place, naming, comprehension, NPI score and HAMD-21 score between 2 groups (P > 0.05, for all). There were no statistical differences in incidence of olfactory dysfunction, threshold of detection and recognition between 2 groups (P > 0.05, for all). There were statistical differences in the incidence of olfactory disorders among different ApoE genotypes (Fisher's exact probability: P = 0.000). To further evaluate the effect of ApoEε4 allele on the olfactory function, subjects were additionally dichotomized according to the presence or absence of at least one ApoEε4 allele. Comparing with the subjects without ApoEε4 allele, the olfactory function decreased significantly in those with ApoEε4 allele (0/11 vs. 12/13; Fisher's exact probability: P = 0.000). Conclusions The patients with 11C-PIB-positive cognitive impairment (AD and MCI) had significant olfactory disturbance, which was related to ApoEε4 allele. The assessment of clinical, genotype and olfactory characteristic was helpful in early diagnosis of AD patients. [ABSTRACT FROM AUTHOR]

The neurosurgeons of PLA General Hospital are making effort to participate in the China Brain Project from the aspects of Science, Technology, Engineering and Medicine, namely "STEM". We initiated the brain research by utilizing central nervous system tumor and other brain diseases as unique study models, and leveraging specific technologies such as neuroimaging, intraoperative electrical stimulation and intracranial electroencephalography. Moreover, we further combine engineering advances with brain-inspired intelligence as well as novel materials to develop minimally invasive or non-invasive brain-computer interface (BCI) devices. With the aim of diagnosis and intervention of Alzheimer's disease (AD) and other major brain diseases, we have used physical neuromodulation (such as sound, light, electricity, magnetism, etc.) for therapeutic treatments of these brain disorders, so as to contribute to the brain research and clinical translation in China in a significant way. [ABSTRACT FROM AUTHOR]

Objective To evaluate the expression of P62 protein in the characteristic pathological changes of common neurodegenerative diseases and to explore its significance in pathological diagnosis. Methods Eleven cases of neurodegenerative diseases and 3 normal controls which were clinically and pathologically diagnosed from June 1994 to October 2017 were included. The neurodegenerative diseases consisted of 5 cases of Alzheimer's disease (AD) and 2 of which were diagnosed as AD combined with argyrophilic grain disease (AGD), 3 cases of Parkinson's disease (PD), 2 cases of progressive supranuclear palsy (PSP) and 1 case of multiple system atrophy (MSA). Three cases without neurological symptoms, signs and brain pathological changes were used as the normal control. Brain tissues were stained with HE, luxol fast blue (LFB) and Gallyas - Braak silver staining, as well as antibodies to amyloid β - protein (A β), AT8, α- synuclein and P62. The staining results were compared under microscope. Results P62 protein was present in the neurofibrillary tangles of AD, in the Lewy body and Lewy neurites of PD, in the tufted astrocyte of PSP, in the argyrophilic grain of AGD and in the glial cytoplasmic inclusion of MSA. The morphological characteristics were consistent with the results of staining with specific antibodies. P62 protein was only expressed in a small amount in the neuritic plaque of AD, and the diffuse plaques were negative. In addition, P62 protein was also deposited in corpora amylacea. No positive pathological structure of P62 immunohistochemical staining was found in normal control brain tissues. Conclusions The P62 protein is expressed in the characteristic pathological changes and corpora amylacea of AD, PD, PSP, MSA and other diseases. Morphological staining results are consistent with histology of various neurodegenerative diseases and corresponding specific protein expression staining results. So the P62 antibody is recommended as the aiding pathological diagnosis of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a kind of central nervous system degenerative disease with higher incidence, which has been paid increasing attention. The pathogenesis is not yet clear though it has been studied a lot. The existing theories focused on amyloid β-protein (Aβ) deposit, hyperphosphorylation of tau and cholinergic neuronal loss. There is mainly symptomatic treatment which cannot reverse disease course. So early diagnosis is particularly important for prevention and treatment of AD. The article will review recent advances in the studies of early diagnosis of AD. It may help accurately diagnose the process from mild cognitive impairment (MCI) to early AD and give advice on prevention and treatment. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is one of most common neurodegenerative diseases, which gradually begins and develops after 65 years old, presenting as progressive and irreversible memory loss and other cognitive decline, and finally causes dementia and disability. Therefore, early diagnosis, timely treatment and effective prevention of AD have been become important clinical and scientific problems. During the period of Twelfth Five-Year Plan for National Economic and Social Development, our team have engaged in AD diagnosis and treatment for a long time and carried out studies in the field of pathogenesis, epidemiology, screening of risk factors, neuropsychological tests, imaging, biomarkers and early intervention of AD. This paper has summarized these research achievements. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) becomes a major disease affecting the elderly with high prevalence. However, no disease-modifying therapies are currently available. AD has long been regarded as a disease of brain itself, but recent studies found that systemic disorders are associated with risk for AD. During the period of Twelfth Five-Year Plan for National Economic and Social Development, our team tried to reveal the pathogenesis, targets, amyloid β-protein (Aβ) clearence pathway and drugs from both central and peripheral approaches, and have discovered: 1) the ratio of p75 neurotrophin receptor (p75NTR) in the brain of AD regulates the over-production and clearence of Aβ in sporadic AD. 2) Peripheral Aβ is able to enter brain, forms AD-type pathologies and induces neuronal deficits, revealing the peripheral mechanism of AD. 3) The effectiveness and safety of brain A β clearance by peripheral organs and tissues has been verified. Based on these findings, we proposed a systemic view of AD, to understand pathogenesis and develop novel diagnostic methods and therapies from a systemic approach. [ABSTRACT FROM AUTHOR]

This paper proposed a graph feature selection method for Alzheimer's disease diagnosis， by adding the information inherent in the observations into a sparse multi-task learning framework. Specifically， this paper firstly defined two relations (i.e.， the feature-feature relation and the sample-sample relation，respectively) based on the prior knowledge. Then embedding these two kinds of relations into a multi-task learning framework (ie.， a least square loss function plus an l2-norm regularization term) to conduct feature selection. Furthermore，it fed the reduced data into a support vector machine (SVM) for conducting the identification of Alzheimer's disease (AD). Finally， the experimental results on a subset of the Alzheimer's disease neuroimaging initiative (ADNI) dataset show the effectiveness o f the proposed method in terms of classification accuracy， by comparing with the state-of-the-art methods， including K nearest neighbor (KNN)， SVM， and so on. This paper proves that the proposed method can improve the performance of AD diagnosis accuracy， by take feature selection and two kinds of relation into account simultaneously. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Contemporary Neurology & Neurosurgery is the property of Chinese Journal of Contemporary Neurology & Neurosurgery and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Contemporary Neurology & Neurosurgery is the property of Chinese Journal of Contemporary Neurology & Neurosurgery and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Contemporary Neurology & Neurosurgery is the property of Chinese Journal of Contemporary Neurology & Neurosurgery and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Contemporary Neurology & Neurosurgery is the property of Chinese Journal of Contemporary Neurology & Neurosurgery and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly. Early diagnosis and prediction plays an important role in early intervention and delaying disease progression of AD. This paper focused on the principles and process of pattern classification method, and its application in the clinical study and auxiliary diagnosis of AD. The biomarkers, neuroimaging and cognitive ability scales are important features for pattern classification. Various classification algorithms including Bayesian networks, decision trees, support vector machines (SVM) and multilayer perception have been adopted to distinguish AD, mild cognitive impairment (MCI) and normal aging subjects. Besides, they can effectively trace and analyze MCI patients. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of tenuigenin (TEN) on expression of brain-derived neurotrophic factor (BDNF), and its receptor tyrosine protein kinase B (TrkB) in the hippocampal CA1 region of Alzheimer's disease (AD) model rats. Methods Sixty male Wistar rats were divided randomly into 4 groups: the control group, the model group, 12.50 mg/ml TEN group and 37.50 mg/ml TEN group. AD model rats were made by injecting ibotenic acid into Meynert basal nuclei of aging rats induced by D-galactose. The expressions of BDNF and its receptor TrkB in the hippocampal CA1 region were measured by immunohistochemistry method. Results The positive expressions of BDNF and TrkB were pale brown and mainly in neuronal cell membrane of the hippocampal CA1 region measured by immunohistochemistry method. The average absorbance values of BDNF and its receptor TrkB in the control group were 0.47 ± 0.02 and 0.46 ± 0.05, while in the model group were 0.30 ± 0.02 and 0.21 ± 0.07 which were significantly lower than that of the control group (P = 0.000, for all). The average absorbance values of BDNF and its receptor TrkB in 12.50 mg/ml TEN group were 0.35 ± 0.05 and 0.32 ± 0.07, which were significantly higher than that of the model group (P = 0.000, for all) and 37.50 mg/ml TEN group were 0.43 ± 0.05 and 0.37 ± 0.03, which were significantly higher than that of the model group (P = 0.000, for all). The average absorbance values of BDNF and its receptor TrkB in 37.50 mg/ml TEN group increased significantly than that in 12.50 mg/ml TEN group (P = 0.000). Conclusions TEN can dose-dependently increase BDNF and its receptor TrkB expression in the hippocampal CA1 region of Alzheimer's disease model rats, which may partly explain the beneficial effects of TEN on cognitive function. [ABSTRACT FROM AUTHOR]

Objective To delineate the cerebral metabolic patterns presented in 18F-FDG PET images in various types of dementia with SPM analysis. Methods Patients who underwent 18F-FDG PET scanning with a retrospectively confirmed diagnosis according to strictly defined clinical research criteria were studied. Clinical follow-up enabled appropriate patient inclusion. A total of 62 patients were included, of which 20 patients were diagnosed as Alzheimer's disease (AD), 20 frontotemporal dementia (FTD), 10 dementia with Lewy body (DLB), 7 progressive supranuclear palsy (PSP), 3 primary progressive aphasia (PPA), 1 corticobasal ganglionic degeneration (CBD), 1 multiple system atrophy (MSA). 18F-FDG PET images of each group were analyzed and compared to 20 healthy controls using SPM5. Results Disease-specific patterns of relatively decreased metabolic activity were found in AD (bilateral parietotemporal regions and frontal regions sparing sensorimotor cortex), FTD (asymmetric frontotemporal regions), DLB (occipital lobe, visual cortex and bilateral superior temporal gyrus), PSP (bilateral dorsolateral prefrontal cortex, anterolateral temporal regions, caudate nucleus and mesencephalon), PPA (Broca's area in left frontal lobe, left temporal cortex excepting posterior superior temporal gyrus, CBD (asymmetricly involved cortical regions, prodominately on right side, around bilateral central sulcus and right basal ganglia), MSA (bilateral cerebellum dorsolateral cortex and left putamen), and right medial temporal cortex). Conclusions Specific dementia related cerebral metabolic patterns in 18F-FDG PET might assist in early differential diagnosis of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) brought about much pressure in modern aging society both economically and psychologically, so it is meaningful to carry out AD research. Being considered as the most successful multi-center, inter-disciplinary and longitudinal research in AD field, Alzheimer's Disease Neuroimaging Initiative (ADNI) has obtained outstanding achievements. In this review, we attempt to introduce the research plan of ADNI project for reference. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD), the most prevalent form of dementia worldwide, can be deemed as the next global health epidemic. The biochemistry underlying deposition of amyloid beta (A β) and hyperphosphorylated tau aggregates in AD has been extensively studied. The oligomeric forms of Aβ that are derived from the normal soluble Aβ peptides are believed to be the most toxic. However, it is the fibrillar Aβ form that aggregates as amyloid plaques and cerebral amyloid angiopathy, which serve as pathological hallmarks of AD. Moreover, deposits of abnormally phosphorylated tau that form soluble toxic oligomers and then accumulate as neurofibrillary tangles are an essential part of AD pathology. Currently, many strategies are being tested that either inhibit, eradicate or prevent the development of plaques in AD. An exciting new approach on the horizon is the immunization approach. Dramatic results from AD animal models have shown promise for active and passive immune therapies targeting A β. However, there is very limited data in humans that suggests a clear benefit. Some hurdles faced with these studies arise from complications noted with therapy. Encephalitis has been reported in trials of active immunization and vasogenic edema or amyloid-related imaging abnormalities (ARIA) has been reported with passive immunization in a minority of patients. As yet, therapies targeting only tau are still limited to mouse models with few studies targeting both pathologies. As the majority of approaches tried so far are based on targeting a self-protein, though in an abnormal conformation, benefits of therapy need to be balanced against the possible risks of stimulating excessive toxic inflammation. For better efficacy, future strategies will need to focus on the toxic oligomers and targeting all aspects of AD pathology. [ABSTRACT FROM AUTHOR]

The word "dementia" originates with Dr. Philippe Pinel of France. Back in 1801, Pinel reported a young female patient, aged 34, who was exhibiting some strange symptoms for someone in her age group. Pinel described this woman's condition as "demence", or an incoherence of mental faculties. It was believed that the term "dementia" came from this association. More than a century later (1906), Dr. Alois Alzheimer published a paper on one of his patients who had very similar symptoms and behaviors as Pinel's patient. This description, of a woman known as Auguste D, was the first scientific report of the disease now known as Alzheimer's disease. It is now clear that Alzheimer's disease is a major cause of dementia in elderly people as well as in relatively young adults. Research in the last two centuries has led to a greatly improved understanding of what Alzheimer's disease is, who gets it, and how it develops and affects the brain. Those works are beginning to pay off with better diagnostic techniques, improved treatments, and even potential ways of preventing these diseases. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly, and is the most common cause of dementia. Epidemiological studies have discovered that, 44% of patients with AD are associated with sleep disorders and (or) circadian rhythm disorders. Now there are growing evidences indicating that interstitial fluid amyloid - β protein (A β) levels exhibit circadian rhythm fluctuation, and sleep disorders will accelerate the process of Aβ deposition, which may act as a risk factor of AD, suggesting the possible reciprocal interaction between sleep disorders and AD. The mechanism is not yet completely clear. Sleep disorders may be related with the impairments of both sleep - wake regulating system, circadian rhythm regulating system and the change of zeitgeber in AD. Sleep disorders would affect neuronal activity, neurotransmitter secretion, and as a stressor affecting A β processing and metabolism, thus accelerate the pathological process of AD. This paper reviewed the progress in the studies of reciprocal interaction between sleep disorders and Alzheimer's disease and the possible mechanisms. [ABSTRACT FROM AUTHOR]