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The ability of the rodent brain to support plasticity-related phenomena declines with increasing age. Here we investigated the extent to which old rats retain the capacity to initiate transcription for immediate early genes, particularly as it relates to brain plasticity, in response to a strong stimulus. The intraperitoneal administration of pentylenetetrazole (PTZ) to rats of various ages evoked tonic-clonic seizures. Using an RNA gel-blot and in situ hybridization analysis, we found that 1 hour after the onset of seizure, messenger RNA (mRNA) for tissue plasminogen activator (TPA) was increased approximately 3.7-fold in the hippocampi of 3-month-old rats. The levels of TPA mRNA in the hippocampi and cortices of 3-month-old rats returned to control levels by 3 hours after PTZ administration. The levels of TPA mRNA increased 2.5-fold in the hippocampi of 18-month-old rats and 1.8-fold in the brains of the 28-month-old-rats at 3 hours and returned to basal levels by 15 hours following PTZ treatment. Quantitatively similar increases were calculated for the cortex. At peak induction the transcripts were localized throughout the cortical layers of the 3-moth-old rats, whereas the TPA mRNA expression was restricted to cortical layer V of the older rats. Our results suggest that although the aging brain retains the capacity to respond to chemically induced seizures, the induction of TPA mRNA is temporarily delayed and the levels are diminished with increasing age. Because TPA has been implicated in neuronal plasticity, this finding suggests that immediate early genes are important factors in the limited plasticity of the aging brain.

Event-related P300 potentials closely reflect cognitive functions such as stimulus discrimination (N250) and processing time (P300 latencies) as well as attention capabilities (P300 amplitudes). To delineate the age-related dynamics of P300 potentials, we investigated 250 healthy subjects between 18 and 98 years of age in a cross-sectional study. A total of P300 visual P300 tests was performed in two different paradigms (PI, passive condition, n = 80; PII, active condition, n = 250). In both P300 paradigms, the N250 and P300 latencies were markedly prolonged (p < . 001) in older age, whereas the N250 and P300 latency differences between PII and PI did not change (p >. 05). The P300 amplitudes in paradigm I and II revealed only a slight age-related reduction. In feet, the P300 amplitude ratios between PII and PI remained constant. Third-order polynomial regressions provided the bestfit of the aging-P300 interactions in paradigms I and II for both males and females. Interestingly, females showed a greater and possibly earlier P300 latency increase during aging than males. These age-related changes of P300 potentials indicate a rather mild cognitive decline that does not accelerate before old and may be different between both sexes.

Because fibronectin (FN) mRNA has been shown to be increased in the brain of old rats and during in vivo and in vitro aging of both endothelial cells and fibroblasts, it was of interest to determine what effect age and caloric restriction have on the ability of liver cells to express FN mRNA. The prevalence of fibronectin mRNA containing the alternatively spliced variant V95 (FN-V95) was examined by RNA gel blot hybridization in the liver of 10 mo, 18-mo, 30-mo ad lib-fed (AL) and 30-mo food-restricted (FR) rats. The transcripts coding for FN-V95 mRNA were well expressed in the liver of 10-mo and 18-mo-old rats. The hybridization signal then increased (1.3-fold, p

Rts were studied to examine if physical training influences cardiac adenylate cyclase functioning and alterations in senescence. Enhanced adenylate cyclase activity and decreased G1 alpha was seen in young rats, but very little was noted in old rats as a result of physical training. Retarded adenylate cyclase and enhanced Gi alpha proteins may contribute to lowered contractility during exercise, and might be involved in heart failure evolvement in aged people.

Background: Age-related brain injuries, including stroke, are a major cause of physical and mental disabilities. Objective: Therefore, studying the basic mechanism underlying functional recovery after brain stroke in aged subjects is of considerable clinical interest. Methods: This review summarizes the effects of age on recovery after stroke in an animal model, with emphasis on the underlying cellular mechanisms. Results: Data from our laboratory and elsewhere indicate that, behaviorally, aged rats were more severely impaired by stroke than young rats, and they also showed diminished functional recovery. Infarct volume did not differ significantly between young and aged animals, but critical differences were apparent in the cytological response to stroke, most notably an age-related acceleration in the development of the glial scar. Early infarct in older rats is associated with premature accumulation of BrdU-positive microglia and astrocytes, persistence of activated oligodendrocytes, a high incidence of neuronal degeneration and accelerated apoptosis. In aged rats, neuroepithelial-positive cells were rapidly incorporated into the glial scar, but these neuroepithelial-like cells did not make a significant contribution to neurogenesis in the infarcted cortex in young or aged animals. The response of plasticity-associated proteins like MAP1B, was delayed in aged rats. Tissue recovery was further delayed by an age-related increase in the amount of the neurotoxic C-terminal fragment of the β-amyloid precursor protein (A-β) at 2 weeks poststroke. Conclusion: The available evidence indicates that the aged brain has the capability to mount a cytoproliferative response to injury, but the timing of the cellular and genetic response to cerebral insult is dysregulated in aged animals, thereby further compromising functional recovery. Elucidating the molecular basis for this phenomenon in the aging brain could yield novel approaches to neurorestoration in the elderly. [ABSTRACT FROM AUTHOR]

Experimental evidence indicates that uraemic patients undergoing haemodialysis are subject to increased oxidative stress. Plasmalogens are a phospholipid subclass found in cell membranes and plasma lipoproteins, which may work as an endogenous antioxidant. Using gas chromatography, we measured reduced portions of fatty aldehyde dimethyl acetals (16:0 DMA and 18:0 DMA, representing derivatives of plasmalogens) in fatty acid patterns of fasting serum phospholipids from 30 patients with chronic renal failure (CRF) receiving repeated ambulatory haemodialysis, as compared to 99 normal control subjects (CS). The highly significant difference of mean 16:0 DMA and 18:0 DMA values between CRF patients and CS (0.53 ± 0.15 vs. 0.67 ± 0.13, p < 0.001 and 0.33 ± 0.11 vs. 0.40 ± 0.11, p < 0.01, respectively) was lost when the patients were compared to subjects older than 85 (16:0 DMA) or 75 years (18:0 DMA). Weak, but significant inverse correlations with age or triglycerides were observed in blood serum of CS for 16:0 DMA and 18:0 DMA, respectively, but not of the patients. Partial correlation analysis indicated a mutually independent association of age and triglyceride values with serum plasmalogens in CS, but not in CRF patients. In conclusion, the reduced content of serum plasmalogen phospholipids of uraemic patients undergoing haemodialysis suggests an increased oxidative stress.Copyright © 2002 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

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