Motor Activity

Publication Title: 
Journal of the American Geriatrics Society

OBJECTIVES: To assess lifestyle factors including physical activity, smoking, alcohol consumption, and dietary habits in men and women with exceptional longevity. DESIGN: Retrospective cohort study. SETTING: A cohort of community-dwelling Ashkenazi Jewish individuals with exceptional longevity defined as survival and living independently at age 95 and older.

Author(s): 
Rajpathak, Swapnil N.
Liu, Yingheng
Ben-David, Orit
Reddy, Saritha
Atzmon, Gil
Crandall, Jill
Barzilai, Nir
Publication Title: 
Neurobiology of Disease

An increasing body of evidence indicates a role for oligomers of the amyloid-? peptide (A?) in the neurotoxicity of this peptide and the pathology of Alzheimer's disease (AD). Several neurotoxic oligomeric forms of A? have been noted ranging from the larger Amyloid ?-Derived Diffusible Ligands (ADDLs) to smaller trimers and dimers of A?. More recently a dodecameric form of A? with a 56 kDa molecular weight, denoted A?*56, was shown to cause memory impairment in AD model mice.

Author(s): 
Scherzer-Attali, R.
Farfara, D.
Cooper, I.
Levin, A.
Ben-Romano, T.
Trudler, D.
Vientrov, M.
Shaltiel-Karyo, R.
Shalev, D. E.
Segev-Amzaleg, N.
Gazit, E.
Segal, D.
Frenkel, D.
Publication Title: 
Human Molecular Genetics

In amyotrophic lateral sclerosis (ALS), the progressive loss of motor neurons is accompanied by extensive muscle denervation, resulting in paralysis and ultimately death. Upregulation of amyloid beta (A4) precursor protein (APP) in muscle fibres coincides with symptom onset in both sporadic ALS patients and the SOD1(G93A) mouse model of familial ALS.

Author(s): 
Bryson, J. Barney
Hobbs, Carl
Parsons, Michael J.
Bosch, Karen D.
Pandraud, Amelie
Walsh, Frank S.
Doherty, Patrick
Greensmith, Linda
Publication Title: 
PloS One

Mutations in the fused in sarcoma/translated in liposarcoma gene (FUS/TLS, FUS) have been identified in sporadic and familial forms of amyotrophic lateral sclerosis (ALS). FUS is an RNA-binding protein that is normally localized in the nucleus, but is mislocalized to the cytoplasm in ALS, and comprises cytoplasmic inclusions in ALS-affected areas. However, it is still unknown whether the neurodegeneration that occurs in ALS is caused by the loss of FUS nuclear function, or by the gain of toxic function due to cytoplasmic FUS aggregation.

Author(s): 
Sasayama, Hiroshi
Shimamura, Mai
Tokuda, Takahiko
Azuma, Yumiko
Yoshida, Tomokatsu
Mizuno, Toshiki
Nakagawa, Masanori
Fujikake, Nobuhiro
Nagai, Yoshitaka
Yamaguchi, Masamitsu
Publication Title: 
Human Molecular Genetics

Niemann-Pick type C (NPC) disease, an autosomal recessive disorder caused primarily by loss-of-function mutations in NPC1 gene, is characterized neuropathologically by intracellular cholesterol accumulation, gliosis and neuronal loss in selected brain regions. Recent studies have shown that NPC disease exhibits intriguing parallels with Alzheimer's disease (AD), including the presence of tau-positive neurofibrillary tangles (NFTs) and ?-amyloid (A?)-related peptides in vulnerable brain regions. Since enhanced cholesterol level, which acts as a risk factor for AD, can increase A?

Author(s): 
Maulik, Mahua
Ghoshal, Bibaswan
Kim, John
Wang, Yanlin
Yang, Jing
Westaway, David
Kar, Satyabrata
Publication Title: 
Gene

Previous studies have shown that polyphenols might be potent neuroprotective agents in Drosophila melanogaster wild type Canton-S acutely or chronically treated with paraquat (PQ), a selective toxin for elimination of dopaminergic (DAergic) neurons by oxidative stress (OS), as model of Parkinson's disease (PD).

Author(s): 
Bonilla-Ramirez, Leonardo
Jimenez-Del-Rio, Marlene
Velez-Pardo, Carlos
Publication Title: 
Genetics

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.

Author(s): 
Petersen, Andrew J.
Katzenberger, Rebeccah J.
Wassarman, David A.
Publication Title: 
InvestigaciÛn ClÌnica

Wilson disease is a hereditary disorder caused by mutations of the ATP7B gene, which leads to intoxication with copper as a result of an unbalance of copper homeostasis. The clinical manifestations resulting from this intoxication are related to the affectation of liver and the encephalon in most cases. Several animal models are currently available for the study of the malady. However, in such models no neurological symptoms are observed, which limits their use for the study of pathogenic effects of this disease on the central nervous system.

Author(s): 
Arcaya, JosÈ Luis
Tejeda, Carlos Mario
Salazar, Ubalguis
Silva, Ernesto JosÈ
Urdaneta, Karla
Varela, Krystal
Publication Title: 
Annals of the New York Academy of Sciences

In a long-term longitudinal study of aging in rhesus monkeys, a primary objective has been to determine the effects of aging and caloric restriction (CR) on behavioral and neural parameters. Through the use of automated devices, locomotor activity can be monitored in the home cages of the monkeys. Studies completed thus far indicate a clear age-related decline in activity consistent with such observations in many other species, including humans. However, no consistent effects of CR on activity have been observed.

Author(s): 
Ingram, D. K.
Chefer, S.
Matochik, J.
Moscrip, T. D.
Weed, J.
Roth, G. S.
London, E. D.
Lane, M. A.
Publication Title: 
The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences

As the only paradigm that has consistently increased life span and inhibited the onset and/or progression of disease, dietary restriction has multiple effects on a variety of organ systems. In this brief review, the goal of the panel was to attempt to understand the role of changes in physical activity and body composition as possible modulators of the life span in experimental animals and humans.

Author(s): 
Poehlman, E. T.
Turturro, A.
Bodkin, N.
Cefalu, W.
Heymsfield, S.
Holloszy, J.
Kemnitz, J.

Pages

Subscribe to RSS - Motor Activity