Protein and Nucleic Acid Content in the Aging Human Brain*

Naber, Dieter; Dahnke, H.-G.

doi:10.1111/j.1365-2990.1979.tb00610.x

Cited by 30 publications

(10 citation statements)

References 21 publications

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“…The results for total RNase activity using three normal control and three AD brain samples examining five regions of the brain (frontal lobe, cingulate gyrus, superior parietal lobe, midtemporal lobe, and occipital lobe) are shown in Table 2. Naber and Dahnke (1979) found lower levels of RNA in grey matter when compared with white matter, and we found that there was less total RNase activity in, grey matter, the levels ranging from 40% to 60% of those observed in white matter. Free RNase activity was again found to be very low (<2% of the total activity) in both A D and normal control brain samples (data not shown).…”

Section: Figuresupporting

confidence: 39%

Role of Ribonuclease and Ribonuclease Inhibitor Activities in Alzheimer's Disease

Jones

Knowler

1989

Journal of Neurochemistry

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It has been suggested that defects in the relationship between ribonuclease and its proteinaceous inhibitor could be a contributory factor in Alzheimer's disease. We have investigated this possibility further by analysing free and bound enzyme activities and the activity of the inhibitor in nine regions of diseased and normal brain. These were chosen to include areas known to be affected by the disease, regions not histologically affected but thought to be involved in the disease process, and areas not thought to be involved in the disease. Neither the enzyme nor its inhibitor is defective in its activities in the chosen areas of Alzheimer's disease brain when compared with those of carefully age-matched controls.

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Section: Figuresupporting

confidence: 39%

Role of Ribonuclease and Ribonuclease Inhibitor Activities in Alzheimer's Disease

Jones

Knowler

1989

Journal of Neurochemistry

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“…MB prevented the age-related decline in protein content of the brain. In the aging human brain (ages from 30 to 90 years old), a decrease of 5–15% in protein content has been previously described [56]. Thus, MB has the potential to improve mitochondrial function in fibroblasts, brain, and heart.…”

Section: Redox Active Agentsmentioning

confidence: 99%

Mitochondrial pharmacology: Electron transport chain bypass as strategies to treat mitochondrial dysfunction

2012

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Mitochondrial dysfunction (primary or secondary) is detrimental to intermediary metabolism. Therapeutic strategies to treat/prevent mitochondrial dysfunction could be valuable for managing metabolic and age-related disorders. Here, we review strategies proposed to treat mitochondrial impairment. We then concentrate on redox-active agents, with mild-redox potential, who shuttle electrons among specific cytosolic or mitochondrial redox-centers. We propose that specific redox agents with mild redox potential (−0.1 V; 0.1 V) improve mitochondrial function because they can readily donate or accept electrons in biological systems, thus they enhance metabolic activity and prevent reactive oxygen species (ROS) production. These agents are likely to lack toxic effects because they lack the risk of inhibiting electron transfer in redox centers. This is different from redox agents with strong negative (−0.4 V; −0.2 V) or positive (0.2 V; 0.4 V) redox potentials who alter the redox status of redox-centers (i.e., become permanently reduced or oxidized). This view has been demonstrated by testing the effect of several redox active agents on cellular senescence. Methylene blue (MB, redox potential ≅10 mV) appears to readily cycle between the oxidized and reduced forms using specific mitochondrial and cytosolic redox centers. MB is most effective in delaying cell senescence and enhancing mitochondrial function in vivo and in vitro. Mild-redox agents can alter the biochemical activity of specific mitochondrial components, which then in response alters the expression of nuclear and mitochondrial genes. We present the concept of mitochondrial electron-carrier bypass as a potential result of mild-redox agents, a method to prevent ROS production, improve mitochondrial function, and delay cellular aging. Thus, mild-redox agents may prevent/delay mitochondria-driven disorders.

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“…Frozen neocortex specimens were homogenized in 10% trichloroacetic acid (TCA); following centrifugation the pellets were washed once with 10% TCA and twice with 3:l ethanol/diethyl ether. RNA was extracted from the washed pellet with 0.3 M KOH at 37°C for 1 h (Naber and Dahnke, 1979). The resulting RNA hydrolysate was assayed spectrophotometrically for total nucleic acid content at 260 nm.…”

Section: Isolation Of Rna From Human Postmortem Neocortexmentioning

confidence: 99%

Characterization of Messenger RNA from the Cerebral Cortex of Control and Alzheimer‐Afflicted Brain

Guillemette

Wong

McLachlan

et al. 1986

Journal of Neurochemistry

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A detailed comparative study of RNA transcripts isolated from the neocortex of control and Alzheimer postmortem brains was made to determine whether morphological changes in the chromatin of Alzheimer neurons and glia, which we reported earlier, are accompanied by changes in the products of transcription. A number of parameters were determined including the yields of total and mRNA per gram of tissue, the relative proportions of polyadenylated [poly(A) +] mRNA in the total RNA, the size distribution of the transcripts and the length of their poly(A) tails, and the nature of their in vitro translation products. The levels of endogenous RNase activity were also measured. The effect of the agonal process on the transcript complement was examined by Northern blotting of a cloned human heat‐shock cDNA to total human brain RNA. Our results reveal that the yields of total RNA, unadenylated mRNA, and poly(A) tail lengths from Alzheimer neocortex samples do not differ significantly from those of control and non Alzheimer dementia neocortex. On the other hand we find a significant reduction in the levels and proportion of poly(A)+ mRNA in the Alzheimer samples as compared to control brain samples. Quantitative rather than qualitative differences were observed in the in vitro translation products when programmed with control and Alzheimer mRNA. No differences were found in the levels of RNase activity between control and Alzheimer simples. Heatshock mRNA transcripts were detected in brain samples from patients in whom fever was associated with death. The direct correlation of reduced poly(A)+ mRNA and chromatin condensation in Alzheimer neocortex suggests a cause‐and‐effect relationship. Whether all transcribed genes are affected or only a specific subset has yet to be determined.

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Protein and Nucleic Acid Content in the Aging Human Brain*

Cited by 30 publications

References 21 publications

Role of Ribonuclease and Ribonuclease Inhibitor Activities in Alzheimer's Disease

Role of Ribonuclease and Ribonuclease Inhibitor Activities in Alzheimer's Disease

Mitochondrial pharmacology: Electron transport chain bypass as strategies to treat mitochondrial dysfunction

Characterization of Messenger RNA from the Cerebral Cortex of Control and Alzheimer‐Afflicted Brain

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