Age-related changes to layer 3 pyramidal cells in the rhesus monkey visual cortex.

The effects of normal aging on morphologic and electrophysiologic properties of layer 3 pyramidal neurons in rhesus monkey primary visual cortex (V1) were assessed with whole-cell, patch-clamp recordings in in vitro slices. In another cohort of monkeys, the ultrastructure of synapses in the layers 2-3 neuropil of V1 was assessed using electron microscopy. Distal apical dendritic branching complexity was reduced in aged neurons, as was the total spine density, due to specific loss of mushroom spines from the apical tree and of thin spines from the basal tree.

Homeostatic responses by surviving cortical pyramidal cells in neurodegenerative tauopathy.

Cortical neuron death is prevalent by 9 months in rTg(tau(P301L))4510 tau mutant mice (TG) and surviving pyramidal cells exhibit dendritic regression and spine loss. We used whole-cell patch-clamp recordings to investigate the impact of these marked structural changes on spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) of layer 3 pyramidal cells in frontal cortical slices from behaviorally characterized TG and non-transgenic (NT) mice at this age. Frontal lobe function of TG mice was intact following a short delay interval but impaired following a long delay interval in an object recognition test, and cortical atrophy and cell loss were pronounced.

Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimer's disease brain.

Neurofibrillary tangles (NFT), intracellular inclusions of abnormal fibrillar forms of microtubule associated protein tau, accumulate in Alzheimer's disease (AD) and other tauopathies and are believed to cause neuronal dysfunction, but the mechanism of tau-mediated toxicity are uncertain. Tau overexpression in cell culture impairs localization and trafficking of organelles. Here we tested the hypothesis that, in the intact brain, changes in mitochondrial distribution occur secondary to pathological changes in tau.

Structural abnormalities in the cortex of the rTg4510 mouse model of tauopathy: a light and electron microscopy study.

rTg4510 transgenic (TG) mice overexpress mutant (P301L) human tau protein. We have compared the dorsal premotor cortex of TG mice versus non-transgenic (NT) mice at 4, 9, and 13 months of age, using light (LM) and electron microscopy (EM). LM assessment shows that cortical thickness in TG mice is reduced by almost 50% from 4 to 13 months of age, while at the same time layer I thickness is reduced by 80%, with most of the cortical thinning occurring between 4 and 9 months.

Effects of normal aging on prefrontal area 46 in the rhesus monkey.

This review is concerned with the effects of normal aging on the structure and function of prefrontal area 46 in the rhesus monkey (Macaca mulatta). Area 46 has complex connections with somatosensory, visual, visuomotor, motor, and limbic systems and a key role in cognition, which frequently declines with age. An important question is what alterations might account for this decline.

Synapses are lost during aging in the primate prefrontal cortex.

An electron microscopic analysis has been carried out on the effects of age on the numerical density of both excitatory (asymmetric) and inhibitory (symmetric) synapses in the neuropil of layers 2/3 and of layer 5 in area 46 from the frontal cortex of behaviorally tested rhesus monkeys. There is no change in the lengths of synaptic junctions with age or in the percentage distribution of synapses relative to the postsynaptic spines and dendritic shafts. However, in layers 2/3 there is an overall loss of about 30% of synapses from 5 to 30 years of age, and both asymmetric and symmetric synapses are lost at the same rate.

Aquatic pollution-induced immunotoxicity in wildlife species.

The potential for chemicals to adversely affect human immunologic health has traditionally been evaluated in rodents, under laboratory conditions. These laboratory studies have generated valuable hazard identification and immunotoxicologic mechanism data; however, genetically diverse populations exposed in the wild may better reflect both human exposure conditions and may provide insight into potential immunotoxic effects in humans. In addition, comparative studies of species occupying reference and impacted sites provide important information on the effects of environmental pollution on the immunologic health of wildlife populations.