Neurodegeneration is a hallmark of the human disease ataxia-telangiectasia (A-T) that is caused by mutation of the A-T mutated (ATM) gene. We have analyzed Drosophila melanogaster ATM mutants to determine the molecular mechanisms underlying neurodegeneration in A-T. Previously, we found that ATM mutants upregulate the expression of innate immune response (IIR) genes and undergo neurodegeneration in the central nervous system. Here, we present evidence that activation of the IIR is a cause of neurodegeneration in ATM mutants.
Is it possible to enhance neural and cognitive function with cognitive training techniques? Can we delay age-related decline in cognitive function with interventions and stave off Alzheimer's disease? Does an aged brain really have the capacity to change in response to stimulation? In the present paper, we consider the neuroplasticity of the aging brain, that is, the brain's ability to increase capacity in response to sustained experience.
Body function rhythmicity has a key function for the regulation of internal timing and adaptation to the environment. A wealth of recent data has implicated endogenous biological rhythm generation and regulation in susceptibility to disease, longevity, cognitive performance. Concerning brain diseases, it has been established that many molecular pathways implicated in neurodegeneration are under circadian regulation. At the molecular level, this regulation relies on clock genes forming interconnected, self-sustained transcriptional/translational feedback loops.
Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons. REST is lost, however, in mild cognitive impairment and Alzheimer's disease.
A common analogy to aging is that of a boulder being worn down to rubble by the unremitting onslaught of time. In contrast, Swaab's "use it or lose it" concept is important because it emphasizes some positive consequences of experience. For example, early exposure to complex experience may offer some protection from "wear and tear" degradation through improvements in vascular support, diet, exercise, and coping with stress. Exposure to complex experience in old age can also generate new synapses in the cerebral cortex and cerebellum.
The insulin-sensitizing drug phenformin, in addition to its clinical utility in type II diabetes, has been reported to lower blood lipids, reduce body fat, enhance cellular immunity, and--in rodents--to increase mean lifespan and retard the development of growth of cancer. Initial studies with the insulin-sensitizing nutrient chromium picolinate indicate that it aids glucose tolerance in type II diabetes, lowers elevated LDL cholesterol, reduces body fat while increasing lean mass, and--in rats--increases median lifespan.
The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
Regression analyses of primate life spans on recently revised female body and brain masses of Old World primates predict a human life span of between 72 years and 91 years-estimates that exceed the age of human menopause (and prior estimates) by well over 20 years. The life spans predicted from body and brain sizes in the early Homo suggest that postreproductive life spans predate Homo sapiens Among anthropoid primates, residual longevity after body and brain effects are controlled is greatest for Homo and for the New World monkeys of the genus Cebus.