Role of apo E in Alzheimer's disease

1994 ◽  
Vol 109 (1-2) ◽  
pp. 335
Author(s):  
K.H. Weisgraber
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apo E

scholarly journals Role of cathepsins in Alzheimer's disease: A systematic review

2018 ◽  
Vol 7 (1) ◽  
pp. 1-10
Author(s):  
S. Rastegar ◽  
A. Nouri ◽  
R. Masoudi ◽  
R. Tavakoli
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Final Analysis ◽  
Beta Amyloid ◽  
Protective Role ◽  
Biomedical Sciences ◽  
C Terminus ◽  
Apo E ◽  
The Subject

Alzheimer's disease (AD) is a multifactorial disease. In addition to the precipitating of two proteins betaamyloid peptide and neurofebrillary tangles, which are the main mechanisms involved in the pathogenesis ofAD, other factors such as inflammatory mechanisms and changes in lysosomal enzymes play an important part in the pathogenesis of this disease. Increased and decreased lysosomal proteases, such as cathepsin, can lead to functional impairment and gradual death of neurons. The aim of this review was to investigate the role of cathepsins in the pathogenesis of AD. To conduct this review, relevant articles published between 2000 and 2016, and indexed in reliable databases including PubMed, Google Scholar, Scopus and Web of Science were retrieved. After reviewing the articles, 30 articles that directly addressed the subject of this review were included in final analysis. Cathepsins exacerbate intracellular conditions in neurons, by processing beta-amyloid precursor protein and converting it into amyloid beta. They also play a protective role against AD and fight it by catalyzing the decomposition of beta-amyloids and converting them into the cut out forms of the carboxyl C-terminus. In addition, the 24 kDa fragment resulting from the effect of cathepsin D on apolipoprotein E (ApoE) is the second binding to the receptor in the ApoE. This fragment may also be the cause of the pathogenicity of Apo E in AD. Identifying and explaining the mechanisms involved in the pathogenesis of AD can play a significant role in the prevention and treatment of this disease. Since cathepsins play a pivotal role in the decomposition of beta-amyloid and reduction of the risk of AD, further studies can be considered an effective approach to study AD.Journal of Medical and Biomedical Sciences (2018) 7(1), 1 - 10

Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hormone Receptor ◽  
Receptor Type ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

Therapeutic role of MSCs-derived exosomes for Alzheimer's disease.

2020 ◽  
Vol 37 (2) ◽  
pp. 1-12
Author(s):  
Sara M. Kamal ◽  
Aliaa R.H. Mostafa ◽  
Sanaa M.R. Wahba
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Role

Exploring the Role of Aggregated Proteomes in the Pathogenesis of Alzheimer’s Disease

2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Early Onset ◽  
Late Onset ◽  
Precursor Protein ◽  
Brain Disorder ◽  
Amyloid Aβ ◽  
T Tau

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.

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