TIME TO THROW IN THE TOWEL?

PEDIATRICS ◽  
1994 ◽  
Vol 93 (6) ◽  
pp. 917-917
Author(s):  
J. F. L.

England must take the credit—or blame—for the reinvention of boxing. The sport was a popular part of the Roman games but had vanished by the 5th century. It returned some 1200 years later, when bare-fist prizefights began to be held in and around London. With help from the Marquess of Queensberry, boxing spread around the world, making money for a considerable number of boxing promoters and a smaller number of boxers. It is appropriate, then, that the British Medical Association should be actively involved in examining the sport. In its latest report, The Boxing Debate, which was issued last week, it repeats its call for a ban on boxing and asks for an independent inquiry into its safety. The briefest reading of the report should persuade even boxing's proponents of the need for an inquiry. In its appendix the report prints abstracts of recent research on what happens to boxers after they have been battered in the ring. For professional boxers, several studies make unpleasant reading. One using computerised tomography found 87 per cent of boxers, in a sample of 18, showed evidence of brain damage. Another records that 15 out of 19 young boxers register as impaired on a battery of neuropsychological tests. Particularly disturbing are three studies which show that changes found in the brains of ex-boxers are immunochemically similar to those seen in Alzheimer's disease. That raises the possibility that even boxers who retire from the ring healthy may pay the price in middle age with early onset of Alzheimer's disease.

2017 ◽  
Vol 13 (7S_Part_16) ◽  
pp. P823-P824
Author(s):  
Mario F. Mendez ◽  
Lorena Montserratt ◽  
Andrew R. Carr ◽  
Elvira E. Jimenez ◽  
Edmond Teng

2014 ◽  
Author(s):  
Joseph P. Barsuglia ◽  
Michelle J. Mather ◽  
Hemali V. Panchal ◽  
Aditi Joshi ◽  
Elvira Jimenez ◽  
...  

2018 ◽  
Author(s):  
Natalia Acosta-Baena ◽  
Carlos Mario Lopera-Gómez ◽  
Mario César Jaramillo-Elorza ◽  
Margarita Giraldo-Chica ◽  
Mauricio Arcos-Burgos ◽  
...  

2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.


2018 ◽  
Vol 15 (8) ◽  
pp. 751-763 ◽  
Author(s):  
Antonio Martinez-Torteya ◽  
Hugo Gomez-Rueda ◽  
Victor Trevino ◽  
Joshua Farber ◽  
Jose Tamez-Pena ◽  
...  

Background: Diagnosing Alzheimer’s disease (AD) in its earliest stages is important for therapeutic and support planning. Similarly, being able to predict who will convert from mild cognitive impairment (MCI) to AD would have clinical implications. Objectives: The goals of this study were to identify features from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database associated with the conversion from MCI to AD, and to characterize the temporal evolution of that conversion. Methods: We screened the publically available ADNI longitudinal database for subjects with MCI who have developed AD (cases: n=305), and subjects with MCI who have remained stable (controls: n=250). Analyses included 1,827 features from laboratory assays (n=12), quantitative MRI scans (n=1,423), PET studies (n=136), medical histories (n=72), and neuropsychological tests (n=184). Statistical longitudinal models identified features with significant differences in longitudinal behavior between cases and matched controls. A multiple-comparison adjusted log-rank test identified the capacity of the significant predictive features to predict early conversion. Results: 411 features (22.5%) were found to be statistically different between cases and controls at the time of AD diagnosis; 385 features were statistically different at least 6 months prior to diagnosis, and 28 features distinguished early from late conversion, 20 of which were obtained from neuropsychological tests. In addition, 69 features (3.7%) had statistically significant changes prior to AD diagnosis. Conclusion: Our results characterized features associated with disease progression from MCI to AD, and, in addition, the log-rank test identified features which are associated with the risk of early conversion.


2020 ◽  
Vol 17 (5) ◽  
pp. 438-445
Author(s):  
Van Giau Vo ◽  
Jung-Min Pyun ◽  
Eva Bagyinszky ◽  
Seong S.A. An ◽  
Sang Y. Kim

Background: Presenilin 1 (PSEN1) was suggested as the most common causative gene of early onset Alzheimer’s Disease (AD). Methods: Patient who presented progressive memory decline in her 40s was enrolled in this study. A broad battery of neuropsychological tests and neuroimaging was applied to make the diagnosis. Genetic tests were performed in the patient to evaluate possible mutations using whole exome sequencing. The pathogenic nature of missense mutation and its 3D protein structure prediction were performed by in silico prediction programs. Results: A pathogenic mutation in PSEN1 (NM_000021.3: c.1027T>C p.Ala285Val), which was found in a Korean EOAD patient. Magnetic resonance imaging scan showed mild left temporal lobe atrophy. Hypometabolism appeared through 18F-fludeoxyglucose Positron Emission Tomography (FDG-PET) scanning in bilateral temporal and parietal lobe, and 18F-Florbetaben-PET (FBB-PET) showed increased amyloid deposition in bilateral frontal, parietal, temporal lobe and hence presumed preclinical AD. Protein modeling showed that the p.Ala285Val is located in the random coil region and could result in extra stress in this region, resulting in the replacement of an alanine residue with a valine. This prediction was confirmed previous in vitro studies that the p.Trp165Cys resulted in an elevated Aβ42/Aβ40 ratio in both COS-1 and HEK293 cell lines compared that of wild-type control. Conclusion: Together, the clinical characteristics and the effect of the mutation would facilitate our understanding of PSEN1 in AD pathogenesis for the disease diagnosis and treatment. Future in vivo study is needed to evaluate the role of PSEN1 p.Ala285Val mutation in AD progression.


Author(s):  
Trang Mai Tong ◽  
Thuy Thi Hong Dao ◽  
Loc Phuoc Doan ◽  
Dat Thanh Nguyen ◽  
Quynh-Tho Thi Nguyen ◽  
...  

2010 ◽  
Vol 468 (1) ◽  
pp. 34-37 ◽  
Author(s):  
Jifeng Guo ◽  
Jiaohua Wei ◽  
Shusheng Liao ◽  
Lei Wang ◽  
Hong Jiang ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document