Evidence for Human Species Longevity to be a Matter of Many Small Adaptations

Why do humans live so much longer than other, short lived species? The researchers here provide evidence to suggest that it is a matter of many small changes, with the specific area of investigation being the the cellular repair mechanisms of autophagy. A world in which differences in longevity between species are the summed contributions from countless small effects is one in which we should discount the possibility that comparative genetic studies - between long-lived and short-lived humans, or between humans and other species - can yield silver bullets, findings that can on their own offer the potential to dramatically improve health and longevity. That expectation, and the sizable mountain of other evidence for the "many tiny contributions" model can be weighed against the recent reports of human PAI-1 mutants with a seven year greater life expectancy than their peers. I wouldn't have wagered on the discovery of such a thing, given what is otherwise known of the genetics of longevity. Research into the importance of protein called p62 shows that a collection of small adaptations in stress activated proteins, accumulated over millennia of human history, could help to explain our increased natural defences and longer lifespan. Many cells in our body, such as those which make up our brain need to last us a lifetime. To do this our cells have developed ways of protecting themselves. One way is through a process called autophagy, which literally means self-e...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs

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AbstractMaintaining genomic stability constitutes a major challenge facing cells. DNA breaks can arise from direct oxidative damage to the DNA backbone, the inappropriate activities of endogenous enzymes such as DNA topoisomerases, or due to transcriptionally-derived RNA/DNA hybrids (R-loops). The progressive accumulation of DNA breaks has been linked to several neurological disorders. Recently, however, several independent studies have implicated nuclear and mitochondrial genomic instability, perturbed co-transcriptional processing, and impaired cellular clearance pathways as causal and intertwined mechanisms underpinning...
Source: Brain - Category: Neurology Source Type: research
In conclusion, the present study demonstrated that TIGIT is a prominent negative immune regulator involved in immunosenescence. This novel finding is highly significant, as targeting TIGIT might be an effective strategy to improve the immune response and decrease age-related comorbidities. Delivery of Extracellular Vesicles as a Potential Basis for Therapies https://www.fightaging.org/archives/2018/01/delivery-of-extracellular-vesicles-as-a-potential-basis-for-therapies/ Here I'll point out a readable open access review paper on the potential use of extracellular vesicles as a basis for therapy: harveste...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Frontotemporal dementia (FTD), the second most common form of dementia in people under 65 years of age, is characterized by progressive atrophy of the frontal and/or temporal lobes. FTD overlaps extensively with the motor neuron disease amyotrophic lateral sclerosis (ALS), especially at the genetic level. Both FTD and ALS can be caused by many mutations in the same set of genes; the most prevalent of these mutations is a GGGGCC repeat expansion in the first intron of C9ORF72. As shown by recent intensive studies, some key cellular pathways are dysregulated in the ALS-FTD spectrum disorder, including autophagy, nucleoc...
Source: EMBO Journal - Category: Molecular Biology Authors: Tags: Molecular Biology of Disease, Neuroscience Review Source Type: research
Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more. This content is...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Nature Neuroscience 20, 1192 (2017). doi:10.1038/nn.4626 Authors: Karl Herrup, Kai-Hei Tse &Hei-Man Chow Hexanucleotide repeat expansions in C9orf72 gene locus create double jeopardy, first by leading to DNA–RNA R-loops that spawn double-strand breaks and second by the synthesis of dipeptide repeats that hinder DNA repair. This two-pronged mechanism may explain neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia.
Source: Nature Neuroscience - Category: Neuroscience Authors: Tags: News and Views Source Type: research
Abstract Cyclin F, encoded by CCNF, is the substrate recognition component of the Skp1-Cul1-F-box E3 ubiquitin ligase complex, SCF(cyclinF). E3 ubiquitin ligases play a key role in ubiquitin-proteasome mediated protein degradation, an essential component of protein homeostatic mechanisms within the cell. By recognising and regulating the availability of several protein substrates, SCF(cyclinF) plays a role in regulating various cellular processes including replication and repair of DNA and cell cycle checkpoint control. Cyclin F dysfunction has been implicated in various forms of cancer and CCNF mutations were rec...
Source: The International Journal of Biochemistry and Cell Biology - Category: Biochemistry Authors: Tags: Int J Biochem Cell Biol Source Type: research
Publication date: Available online 15 May 2017 Source:Journal of Clinical Neuroscience Author(s): Kazuko Hayashi, Ryuhei Araki, Akiko Tanaka Recently, the cognitive abilities of patients with amyotrophic lateral sclerosis (ALS) have been found to be impaired along with the neurodegeneration of motor neurons. Electroencephalography (EEG) of end-stage ALS patients has reportedly shown specific features based on neuronal network modulations, differing from EEG of other patients with cognitive failure and dementia. However, EEG of end-stage ALS patients during anaesthesia has not yet been reported. A 64-year-old male ALS pati...
Source: Journal of Clinical Neuroscience - Category: Neuroscience Source Type: research
This study demonstrates that TNTs play a significant part in the intercellular transfer of α-synuclein fibrils and reveals the specific role of lysosomes in this process. This represents a major breakthrough in understanding the mechanisms underlying the progression of synucleinopathies. These compelling findings, together with previous reports from the same team, point to the general role of TNTs in the propagation of prion-like proteins in neurodegenerative diseases and identify TNTs as a new therapeutic target to combat the progression of these incurable diseases. Shorter Period of Rapamycin Treatment in...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Valosin-containing protein/p97(VCP) is a hexameric ATPase vital to protein degradation during endoplasmic reticulum stress. It regulates diverse cellular functions including autophagy, chromatin remodeling, and DNA repair. In addition, mutations in VCP cause inclusion body myopathy, Paget disease of the bone, and frontotemporal dementia (IBMPFD), as well as amyotrophic lateral sclerosis. Nevertheless, how the VCP activities were regulated and how the pathogenic mutations affect the function of VCP during stress are not unclear. Here we show that the small ubiquitin-like modifier (SUMO)-ylation of VCP is a normal stress res...
Source: Journal of Biological Chemistry - Category: Chemistry Authors: Tags: Molecular Bases of Disease Source Type: research
This article is part of the Frontotemporal Dementia special issue. The two major RNA Binding Proteins involved in Amyotrophic Lateral Sclerosisi and Frontotemporal Dementia are TDP‐43 and FUST/TLS. Both proteins are involved in regulating all aspects of RNA and RNA life cycle within neurons, from transcription, processing, and transport/stability to the formation of cytoplasmic and nuclear stress granules. For this reason, the aberrant aggregation of these factors during disease can impair multiple RNA metabolic pathways and eventually lead to neuronal death/inactivation. The purpose of this review is to provide an up...
Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: Review Source Type: research
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