scholarly journals Probing the correlation of neuronal loss, neurofibrillary tangles, and cell death markers across the Alzheimer's disease Braak stages: a quantitative study in humans

2018 ◽  
Vol 61 ◽  
pp. 1-12 ◽  
Author(s):  
Panos Theofilas ◽  
Alexander J. Ehrenberg ◽  
Austin Nguy ◽  
Julia M. Thackrey ◽  
Sara Dunlop ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Quantitative Study ◽  
Neurofibrillary Tangles ◽  
Neuronal Loss

MicroRNA in Alzheimer’s disease revisited: implications for major neuropathological mechanisms

2018 ◽  
Vol 29 (2) ◽  
pp. 161-182 ◽  
Author(s):  
Reihaneh Dehghani ◽  
Farzaneh Rahmani ◽  
Nima Rezaei
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Neural Plasticity ◽  
Amyloid Β ◽  
Neuronal Loss ◽  
Active Role ◽  
Search Term ◽  
The Central Nervous System ◽  
Irregular Cell

AbstractPathology of Alzheimer’s disease (AD) goes far beyond neurotoxicity resulting from extracellular deposition of amyloid β (Aβ) plaques. Aberrant cleavage of amyloid precursor protein and accumulation of Aβ in the form of the plaque or neurofibrillary tangles are the known primary culprits of AD pathogenesis and target for various regulatory mechanisms. Hyper-phosphorylation of tau, a major component of neurofibrillary tangles, precipitates its aggregation and prevents its clearance. Lipid particles, apolipoproteins and lipoprotein receptors can act in favor or against Aβ and tau accumulation by altering neural membrane characteristics or dynamics of transport across the blood-brain barrier. Lipids also alter the oxidative/anti-oxidative milieu of the central nervous system (CNS). Irregular cell cycle regulation, mitochondrial stress and apoptosis, which follow both, are also implicated in AD-related neuronal loss. Dysfunction in synaptic transmission and loss of neural plasticity contribute to AD. Neuroinflammation is a final trail for many of the pathologic mechanisms while playing an active role in initiation of AD pathology. Alterations in the expression of microRNAs (miRNAs) in AD and their relevance to AD pathology have long been a focus of interest. Herein we focused on the precise pathomechanisms of AD in which miRNAs were implicated. We performed literature search through PubMed and Scopus using the search term: (‘Alzheimer Disease’) OR (‘Alzheimer’s Disease’) AND (‘microRNAs’ OR ‘miRNA’ OR ‘MiR’) to reach for relevant articles. We show how a limited number of common dysregulated pathways and abnormal mechanisms are affected by various types of miRNAs in AD brain.

scholarly journals Mechanisms of Neuronal Death in the Cerebral Cortex during Aging and Development of Alzheimer’s Disease-Like Pathology in Rats

2019 ◽  
Vol 20 (22) ◽  
pp. 5632 ◽  
Author(s):  
Darya V. Telegina ◽  
Gleb K. Suvorov ◽  
Oyuna S. Kozhevnikova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Decision Making ◽  
Cell Death ◽  
Cerebral Cortex ◽  
Brain Development ◽  
Brain Region ◽  
Neuronal Death ◽  
Neuronal Loss ◽  
Decision Making Behavior

Alzheimer’s disease (AD) is the commonest type of late-life dementia and damages the cerebral cortex, a vulnerable brain region implicated in memory, emotion, cognition, and decision-making behavior. AD is characterized by progressive neuronal loss, but the mechanisms of cell death at different stages of the disease remain unknown. Here, by means of OXYS rats as an appropriate model of the most common (sporadic) AD form, we studied the main pathways of cell death during development of AD-like pathology, including the preclinical stage. We found that apoptosis is activated at the pre-symptomatic stage (age 20 days) correlating with the retardation of brain development in the OXYS strain early in life. Progression of the AD-like pathology was accompanied by activation of apoptosis and necroptosis resulting from a decline of autophagy-mediated proteostasis. Our results are consistent with the idea that the nature of changes in the pathways of apoptosis, autophagy, and necrosis depends on the stage of AD.

Effects of a tacrine-8-hydroxyquinoline hybrid (IQM-622) on Aβ accumulation and cell death: Involvement in hippocampal neuronal loss in Alzheimer's disease

2012 ◽  
Vol 46 (3) ◽  
pp. 682-691 ◽  
Author(s):  
Desiree Antequera ◽  
Marta Bolos ◽  
Carlos Spuch ◽  
Consuelo Pascual ◽  
Isidro Ferrer ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Neuronal Loss

Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease

1997 ◽  
Vol 41 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Teresa Gómez-Isla ◽  
Richard Hollister ◽  
Howard West ◽  
Stina Mui ◽  
John H. Growdon ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Neuronal Loss

scholarly journals Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?

2009 ◽  
Vol 3 (3) ◽  
pp. 188-194 ◽  
Author(s):  
Vanessa de Jesus R. de Paula ◽  
Fabiana Meira Guimarães ◽  
Breno Satler Diniz ◽  
Orestes Vicente Forlenza
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangles ◽  
Tau Protein ◽  
Psychological Symptoms ◽  
Senile Plaques ◽  
Memory Loss ◽  
Neuronal Loss ◽  
Personality Changes ◽  
Integrative View

Abstract Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, including memory loss, behavioral and psychological symptoms and personality changes. The neuropathological hallmarks of AD are the presence of neuritic (senile) plaques (NP) and neurofibrillary tangles (NFT), along with neuronal loss, dystrophic neurites, and gliosis. Neuritic plaques are extracellular lesions and their main constituent is the amyloid-b42 peptide (Ab42). Neurofibrillary tangles are intracellular lesions that are mainly composed of hyperphosphorylated TAU protein. In this article, we review the major hypotheses concerning the physiopathology of AD, focusing on the b-amyloid cascade as primary events (supported by the "baptists") and cytoskeletal abnormalities secondary to the hyperphosphorylation of protein TAU (as advocated by the "Tauists"). We further provide an integrative view of the physiopathology of AD.

scholarly journals Implication of Adult Hippocampal Neurogenesis in Alzheimer’s Disease and Potential Therapeutic Approaches

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 286
Author(s):  
Hesham Essa ◽  
Lee Peyton ◽  
Whidul Hasan ◽  
Brandon Emanuel León ◽  
Doo-Sup Choi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dentate Gyrus ◽  
Neurofibrillary Tangles ◽  
Neuronal Loss ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Key Factors ◽  
App Gene

Alzheimer’s disease is the most common neurodegenerative disease, affecting more than 6 million US citizens and representing the most prevalent cause for dementia. Neurogenesis has been repeatedly reported to be impaired in AD mouse models, but the reason for this impairment remains unclear. Several key factors play a crucial role in AD including Aβ accumulation, intracellular neurofibrillary tangles accumulation, and neuronal loss (specifically in the dentate gyrus of the hippocampus). Neurofibrillary tangles have been long associated with the neuronal loss in the dentate gyrus. Of note, Aβ accumulation plays an important role in the impairment of neurogenesis, but recent studies started to shed a light on the role of APP gene expression on the neurogenesis process. In this review, we will discuss the recent approaches to neurogenesis in Alzheimer disease and update the development of therapeutic methods.

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