Mitoenergetic failure in Alzheimer disease.

Mitoenergetic failure in Alzheimer disease. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Mitoenergetic failure in Alzheimer disease. Abstract Text:

Mordhwaj S Parihar,Gregory J Brewer,

Brain cells are highly energy dependent for maintaining ion homeostasis during high metabolic activity. During active periods, full mitochondrial function is essential to generate ATP from electrons that originate with the oxidation of NADH. Decreasing brain metabolism is a significant cause of cognitive abnormalities of Alzheimer disease (AD), but it remains uncertain whether this is the cause of further pathology or whether synaptic loss results in a lower energy demand. Synapses are the first to show pathological symptoms in AD before the onset of clinical symptoms. Because synaptic function has high energy demands, interruption in mitochondrial energy supply could be the major factor in synaptic failure in AD. A newly discovered age-related decline in neuronal NADH and redox ratio may jeopardize this function. Mitochondrial dehydrogenases and several mutations affecting energy transfer are frequently altered in aging and AD. Thus, with the accumulation of genetic defects in mitochondria at the level of energy transfer, the issue of neuronal susceptibility to damage as a function of age and age-related disease becomes important. In an aging rat neuron model, mitochondria are both chronically depolarized and produce more reactive oxygen species with age. These concepts suggest that multiple treatment targets may be needed to reverse this multifactorial disease. This review summarizes new insights based on the interaction of mitoenergetic failure, glutamate excitotoxicity, and amyloid toxicity in the exacerbation of AD.

Mitoenergetic failure in Alzheimer disease. Publishing Authors By Initials

MS Parihar,GJ Brewer,

For similar cells: cellular structures: intracellular space: cytoplasm: cytoplasmic structures: organelles: mitochondria research abstracts see: cells: cellular structures: intracellular space: cytoplasm: cytoplasmic structures: organelles: mitochondria research

PUBMED ID PMID:

MEDLINE DATE:

Mitoenergetic failure in Alzheimer disease. Journal Published:

PUBLICATION TYPE: Review

Journal: American journal of physiology. Cell physiology

VOLUME: 292

Page Numbers: C8-23

Journal Abbreviation: Am. J. Physiol., Cell Physiol.

ISSN: 0363-6143

DAY: 28

MONTH: 06

YEAR: 2006

Mitoenergetic failure in Alzheimer disease. Information

Number of References: 277

LANGUAGE: eng

NlmUniqueID: 100901225

Mitoenergetic failure in Alzheimer disease. Keywords Mesh Terms:

KEYWORDS: Mitochondria

MESH TERMS: metabolism

Chemical & Substance for Abstract: Mitoenergetic failure in Alzheimer disease. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Mitoenergetic failure in Alzheimer disease.

AFFILIATION: Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL 62794-9626, USA.

Country: United States

AGENCY: United States NIA

GRANT: R01 AG 13435

ACRONYM: AG

MEDLINETA: Am J Physiol Cell Physiol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Mitoenergetic failure in Alzheimer disease Related Publications

• A brand new mechanism for copper toxicity.
• A peripatetic pediatrician's journey into pediatric rheumatology: part III.
• An alcohol oxidase dipstick rapidly detects methanol in the serum of mice.
• Analysis of auditory phenotype and karyotype in 200 females with Turner syndrome.
• Association between tetracycline or doxycycline and hepatotoxicity: a population based case-control study.
• Binding studies of alpha-GalNAc-specific lectins to the alpha-GalNAc (Tn-antigen) form of porcine submaxillary mucin and its smaller fragments.
• Brucellosis in general practice.
• Circadian organization of tau mutant hamsters: aftereffects and splitting.
• Competitive binding of AUF1 and TIAR to MYC mRNA controls its translation.
• Coordinate regulation of phospholipid biosynthesis and secretory pathway gene expression in XBP-1(S)-induced endoplasmic reticulum biogenesis.
• Designing lipid nanostructures for local delivery of biologically active macromolecules.
• Diazo preparation via dehydrogenation of hydrazones with "activated" DMSO.
• Director of safe staffing unit can't solve all issues. Interview by Teresa O'Connor.
• Effect of natural antioxidants on oxidative stability of cooked, refrigerated beef and pork.
• Effects of torcetrapib in patients at high risk for coronary events.
• HDL metabolism and the role of HDL in the treatment of high-risk patients with cardiovascular disease.
• In vivo inhibition of E. coli growth by a Ru(II)/Pt(II) supramolecule [(tpy)RuCl(dpp)PtCl2](PF6).
• Local environmental effects and spatial effects in macroecological studies using mapped abundance classes: the case of the rook Corvus frugilegus in Scotland.
• Mapping yeast origins of replication via single-stranded DNA detection.
• Metabolic toxemia of late pregnancy: a disease entity.
• Mitoenergetic failure in Alzheimer disease.
• Part A - microRNAs: discovery, analyses, targets.
• Quality changes in beef gluteus medius, infraspinatus, psoas major, rectus femoris, and teres major enhanced prior to aging.
• Simultaneous age-related depolarization of mitochondrial membrane potential and increased mitochondrial reactive oxygen species production correlate with age-related glutamate excitotoxicity in rat hippocampal neurons.
• The importance of being we: human nature and intergroup relations.
• The independent yet synergistic effects of heparin and dextran.
• The unfolded protein response of B-lymphocytes: PERK-independent development of antibody-secreting cells.
• Tips and techniques for engaging and managing the reluctant, resistant or hostile young person.
• Understanding drug addiction: a neuropsychological perspective.
• Visual field maps in human cortex.