scholarly journals Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

2017 ◽  
Vol 06 (01) ◽  
pp. 1-12 ◽  
Author(s):  
W. John Martin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cellular Energy

scholarly journals What can 7T sodium MRI tell us about cellular energy depletion and neurotransmission in Alzheimer's disease?

2021 ◽  
Author(s):  
Alexa Haeger ◽  
Michel Bottlaender ◽  
Julien Lagarde ◽  
Renata Porciuncula Baptista ◽  
Cécile Rabrait‐Lerman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Energy Depletion ◽  
Sodium Mri ◽  
Cellular Energy

scholarly journals Mitophagy in Alzheimer’s Disease and Other Age-Related Neurodegenerative Diseases

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 150 ◽  
Author(s):  
Qian Cai ◽  
Yu Young Jeong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Cellular Energy ◽  
Age Related ◽  
Mitochondrial Turnover ◽  
Neuronal Functions ◽  
Lateral Sclerosis

Mitochondrial dysfunction is a central aspect of aging and neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Mitochondria are the main cellular energy powerhouses, supplying most of ATP by oxidative phosphorylation, which is required to fuel essential neuronal functions. Efficient removal of aged and dysfunctional mitochondria through mitophagy, a cargo-selective autophagy, is crucial for mitochondrial maintenance and neuronal health. Mechanistic studies into mitophagy have highlighted an integrated and elaborate cellular network that can regulate mitochondrial turnover. In this review, we provide an updated overview of the recent discoveries and advancements on the mitophagy pathways and discuss the molecular mechanisms underlying mitophagy defects in Alzheimer’s disease and other age-related neurodegenerative diseases, as well as the therapeutic potential of mitophagy-enhancing strategies to combat these disorders.

scholarly journals ALZHEIMER’S DISEASE: A CONSEQUENCE OF IMPAIRED MITOPHAGY?

2019 ◽  
pp. 75-80
Author(s):  
VIVEK SHARMA
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Proper Function ◽  
Neuronal Viability ◽  
Cellular Energy ◽  
Mitochondrial Homeostasis ◽  
Neuronal Homeostasis ◽  
Age Related ◽  
Characteristic Features

Neurodegenerative disorders involve complexities of the pathologies, characterized by the progressive loss of neuronal viability, leading to severe physical and cognitive impairments in affected patients. These disorders although may differ in clinical outcomes yet they share common features such as aggregation of neurotoxic metabolites and perturbed cellular and neuronal homeostasis. Mitochondrion is an indispensable organelle for neuronal survival, and its role and place have become critical in research arena of aging and neurodegenaration. The accumulation of damaged mitochondria has been linked to normal aging and multiple age-related disorders including Alzheimer’s disease (AD). Survival and proper function of mitochondria depend on several attributes that include mitochondrial biogenesis and fusion and fission. Mitophagy is an utmost requirement for degradation and removal of damaged mitochondria where the target mitochondria are identified by the autophagosomes and delivered to the lysosome for degradation. Mitophagy plays important roles in mitochondrial homeostasis, neuroprotection, and resistance to neurodegeneration. AD besides other characteristic features involves mitochondrial dysfunctional, bioenergetic deficit, and altered mitophagy. The autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is compromised in AD, resulting in the accumulation of dysfunctional mitochondria that contribute to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits. The present work reviews the various implications of mitophagy in relevance to the pathology of AD.

scholarly journals Hypothesis and Theory: Characterizing Abnormalities of Energy Metabolism Using a Cellular Platform as a Personalized Medicine Approach for Alzheimer’s Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Woo-In Ryu ◽  
Bruce M. Cohen ◽  
Kai-C. Sonntag
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Personalized Medicine ◽  
Preventive Intervention ◽  
Late Onset ◽  
Critical Role ◽  
Cellular Energy ◽  
Cell Functions ◽  
Inflammatory Processes ◽  
Induced Pluripotent

Sporadic or late-onset Alzheimer’s disease (LOAD) is characterized by slowly progressive deterioration and death of CNS neurons. There are currently no substantially disease-modifying therapies. LOAD pathology is closely related to changes with age and include, among others, accumulation of toxic molecules and altered metabolic, microvascular, biochemical and inflammatory processes. In addition, there is growing evidence that cellular energy deficits play a critical role in aging and LOAD pathophysiology. However, the exact mechanisms and causal relationships are largely unknown. In our studies we tested the hypothesis that altered bioenergetic and metabolic cell functions are key elements in LOAD, using a cellular platform consisting of skin fibroblasts derived from LOAD patients and AD-unaffected control individuals and therefrom generated induced pluripotent stem cells that are differentiated to brain-like cells to study LOAD pathogenic processes in context of age, disease, genetic background, cell development, and cell type. This model has revealed that LOAD cells exhibit a multitude of bioenergetic and metabolic alterations, providing evidence for an innate inefficient cellular energy management in LOAD as a prerequisite for the development of neurodegenerative disease with age. We propose that this cellular platform could ultimately be used as a conceptual basis for a personalized medicine tool to predict altered aging and risk for development of dementia, and to test or implement customized therapeutic or disease-preventive intervention strategies.

Plasma metabolites related to cellular energy metabolism are altered in adults with Down syndrome and Alzheimer's disease

2019 ◽  
Vol 79 (7) ◽  
pp. 622-638 ◽  
Author(s):  
Thomas J. Gross ◽  
Eric Doran ◽  
Amrita K. Cheema ◽  
Elizabeth Head ◽  
Ira T. Lott ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Energy Metabolism ◽  
Plasma Metabolites ◽  
Cellular Energy ◽  
Cellular Energy Metabolism

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.

Formation of paired helical filaments in Alzheimer's disease

1984 ◽  
Vol 42 ◽  
pp. 302-303
Author(s):  
J. Metuzals ◽  
D. F. Clapin ◽  
V. Montpetit
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Lobe ◽  
Giant Axon ◽  
Paired Helical Filaments ◽  
Normal Brain ◽  
Protein Assemblies ◽  
Electron Microscopic ◽  
Helical Symmetry ◽  
Structural Levels

Information on the conformation of paired helical filaments (PHF) and the neurofilamentous (NF) network is essential for an understanding of the mechanisms involved in the formation of the primary lesions of Alzheimer's disease (AD): tangles and plaques. The structural and chemical relationships between the NF and the PHF have to be clarified in order to discover the etiological factors of this disease. We are investigating by stereo electron microscopic and biochemical techniques frontal lobe biopsies from patients with AD and squid giant axon preparations. The helical nature of the lesion in AD is related to pathological alterations of basic properties of the nervous system due to the helical symmetry that exists at all hierarchic structural levels in the normal brain. Because of this helical symmetry of NF protein assemblies and PHF, the employment of structure reconstruction techniques to determine the conformation, particularly the handedness of these structures, is most promising. Figs. 1-3 are frontal lobe biopsies.

Computer-aided methods for 3-D visualization of serial sections and thick biological specimens

1992 ◽  
Vol 50 (2) ◽  
pp. 1060-1061
Author(s):  
Mark Ellisman ◽  
Maryann Martone ◽  
Gabriel Soto ◽  
Eleizer Masliah ◽  
David Hessler ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Three Dimensional ◽  
Neuritic Plaque ◽  
Dimensional Structure ◽  
Data Sets ◽  
Molecular Physiology ◽  
Research Activities ◽  
Computer Aided ◽  
Dimensional Reconstruction

Structurally-oriented biologists examine cells, tissues, organelles and macromolecules in order to gain insight into cellular and molecular physiology by relating structure to function. The understanding of these structures can be greatly enhanced by the use of techniques for the visualization and quantitative analysis of three-dimensional structure. Three projects from current research activities will be presented in order to illustrate both the present capabilities of computer aided techniques as well as their limitations and future possibilities.The first project concerns the three-dimensional reconstruction of the neuritic plaques found in the brains of patients with Alzheimer's disease. We have developed a software package “Synu” for investigation of 3D data sets which has been used in conjunction with laser confocal light microscopy to study the structure of the neuritic plaque. Tissue sections of autopsy samples from patients with Alzheimer's disease were double-labeled for tau, a cytoskeletal marker for abnormal neurites, and synaptophysin, a marker of presynaptic terminals.

Sign in / Sign up

Export Citation Format

Share Document