All Stories

  1. Muscle Ageing and Sarcopenia Study (MASS) Lifecourse: a valuable resource for understanding skeletal muscle ageing
  2. Contribution of Nova-classified ultraprocessed foods to energy and nutrient intakes in very old people: the Newcastle 85+ Study
  3. Muscle Ageing and Sarcopenia Study (MASS) Lifecourse: a unique resource for understanding skeletal muscle ageing across adulthood
  4. Ageing of human myofibres in the Vastus Lateralis muscle: a narrative review
  5. Cross-sectional and longitudinal associations between glycaemic measures and grip strength in people without diabetes in the UK Biobank cohort study
  6. Nutrition in the prevention and treatment of skeletal muscle ageing and sarcopenia: a single nutrient, a whole food and a whole diet approach
  7. Identifying combinations of long-term conditions associated with sarcopenia: a cross-sectional decision tree analysis in the UK Biobank study
  8. Hallmarks of ageing in human skeletal muscle and implications for understanding the pathophysiology of sarcopenia in women and men
  9. The prevalence of sarcopenia in Parkinson’s disease and related disorders- a systematic review
  10. Determining the feasibility of characterising cellular senescence in human skeletal muscle and exploring associations with muscle morphology and physical function at different ages: findings from the MASS_Lifecourse Study
  11. New Horizons in cellular senescence for clinicians
  12. Milk intake across adulthood and muscle strength decline from mid- to late life: the MRC National Survey of Health and Development
  13. Immunosenescence profiles are not associated with muscle strength, physical performance and sarcopenia risk in very old adults: The Newcastle 85+ Study
  14. Feasibility and acceptability of a milk and resistance exercise intervention to improve muscle function in community-dwelling older adults (MIlkMAN): Pilot study
  15. <p>Milk for Skeletal Muscle Health and Sarcopenia in Older Adults: A Narrative Review</p>
  16. Effects of dietary patterns and low protein intake on sarcopenia risk in the very old: The Newcastle 85+ study
  17. Study of the Older Adults’ Motivators and Barriers Engaging in a Nutrition and Resistance Exercise Intervention for Sarcopenia: An Embedded Qualitative Project in the MIlkMAN Pilot Study
  18. Sarcopenia, long‐term conditions, and multimorbidity: findings from UK Biobank participants
  19. Mediterranean diet adherence and cognitive function in older UK adults: the European Prospective Investigation into Cancer and Nutrition–Norfolk (EPIC-Norfolk) Study
  20. Milk and resistance exercise intervention to improve muscle function in community-dwelling older adults at risk of sarcopenia (MIlkMAN): protocol for a pilot study
  21. Factors associated with change in self-reported physical activity in the very old: The Newcastle 85+ study
  22. Contribution of protein intake and its interaction with physical activity to transitions between disability states and to death in very old adults: the Newcastle 85+ Study
  23. Dietary Patterns, Skeletal Muscle Health, and Sarcopenia in Older Adults
  24. The recent secular trend in grip strength among older adults: findings from the English Longitudinal Study of Ageing
  25. Low protein intake, muscle strength and physical performance in the very old: The Newcastle 85+ Study
  26. Protein Intake and Disability Trajectories in Very Old Adults: The Newcastle 85+ Study
  27. Mitochondrial respiratory chain function and content are preserved in the skeletal muscle of active very old men and women
  28. Plasma Vitamin B12, Supplementation and Mortality
  29. Mitotic defects lead to neuronal aneuploidy and apoptosis in frontotemporal lobar degeneration caused by MAPT mutations
  30. Nutrition in the Very Old
  31. Elevated Total Homocysteine in All Participants and Plasma Vitamin B12 Concentrations in Women Are Associated With All-Cause and Cardiovascular Mortality in the Very Old: The Newcastle 85+ Study
  32. Factors Associated With Physical Performance Measures in a Multiethnic Cohort of Older Adults
  33. Vitamin D and Ageing
  34. Homocysteine, Tryptophan, and Cognition in the Very Old
  35. Prevalence and determinants of low protein intake in very old adults: insights from the Newcastle 85+ Study
  36. One-Carbon Metabolism Biomarkers and Cognitive Decline in the Very Old: The Newcastle 85+ Study
  37. [P2–140]: ABNORMAL CHROMOSOME COPY NUMBER AND ASSOCIATED NEURONAL CELL DEATH IN FRONTOTEMPORAL LOBAR DEGENERATION
  38. Mitochondrial respiratory chain deficiency in older men and its relationship with muscle mass and performance
  39. Longitudinal changes in global and domain specific cognitive function in the very-old: findings from the Newcastle 85+ Study
  40. Grip strength and inflammatory biomarker profiles in very old adults
  41. Initial level and rate of change in grip strength predict all-cause mortality in very old adults
  42. Vitamin D Status, Muscle Strength and Physical Performance Decline in Very Old Adults: A Prospective Study
  43. Association of mitochondrial respiratory chain deficiency in older men with muscle mass and physical performance: findings from the Hertfordshire Sarcopenia Study
  44. Using Fluorescence In Situ Hybridization (FISH) Analysis to Measure Chromosome Instability and Mosaic Aneuploidy in Neurodegenerative Diseases
  45. Prevalence and incidence of sarcopenia in the very old: findings from the Newcastle 85+ Study
  46. Predicting Risk of Cognitive Decline in Very Old Adults Using Three Models: The Framingham Stroke Risk Profile; the Cardiovascular Risk Factors, Aging, and Dementia Model; and Oxi-Inflammatory Biomarkers
  47. Grip Strength Decline and Its Determinants in the Very Old: Longitudinal Findings from the Newcastle 85+ Study
  48. Micronutrient intake and food sources in the very old: analysis of the Newcastle 85+ Study
  49. What do we know about the nutritional status of the very old? Insights from three cohorts of advanced age from the UK and New Zealand
  50. Macronutrient intake and food sources in the very old: analysis of the Newcastle 85+ Study
  51. Effect of Dietary Patterns on Muscle Strength and Physical Performance in the Very Old: Findings from the Newcastle 85+ Study
  52. Dietary patterns and cognitive functioning in very old adults
  53. Role of Trisomy 21 Mosaicism in Sporadic and Familial Alzheimer's Disease
  54. Dietary Patterns and Socioeconomic Status in the Very Old: The Newcastle 85+ Study
  55. Serum 25-hydroxyvitamin D concentration and its determinants in the very old: the Newcastle 85+ Study
  56. Antihypertensive drug use and risk of cognitive decline in the very old
  57. Is There an Association Between Metabolic Syndrome and Cognitive Function in Very Old Adults? The Newcastle 85+ Study
  58. Serum 25‐hydroxyvitamin D and cognitive decline in the very old: the Newcastle 85+ Study
  59. P2‐011: Aβ INHIBITION OF KINESIN 5 DISRUPTS THE LOCALIZATION AND FUNCTION OF MEMBRANE PROTEINS: IMPLICATIONS FOR NEURONAL RESPONSES TO NEUROTROPHINS, NEUROTRANSMITTERS, GLUCOSE, AND LIPIDS IN AD
  60. 25‐hydroxyvitamin D and increased all‐cause mortality in very old women: the Newcastle 85+ study
  61. P1–118: Frontemporal dementia mutations in MAPT cause chromosome mis‐segregation and aneuploidy including trisomy 21
  62. Mitotic Spindle Defects and Chromosome Mis-Segregation Induced by LDL/Cholesterol—Implications for Niemann-Pick C1, Alzheimer’s Disease, and Atherosclerosis
  63. Midlife dietary patterns and mortality in the population-based study of Swedish twins
  64. P3‐036: Aß inhibition of kinesin 5 induces neurotransmitter and neurotrophin receptor mislocalization and dysfunction
  65. P2‐085: Genomic damage induced by lipoproteins/cholesterol: Implications for Alzheimer's and cardiovascular disease
  66. Down Syndrome Model of Alzheimer’s Disease: Beyond Trisomy 21Nondisjunction
  67. P4‐324: Aβ inhibits specific kinesin motors involved in both mitosis and neuronal function; potential implications for neurogenesis and neuroplasticity in Alzheimer's disease and Down syndrome
  68. Alzheimer Aβ disrupts the mitotic spindle and directly inhibits mitotic microtubule motors
  69. Everyday reasoning abilities in persons with Parkinson's disease
  70. P4‐005: Alzheimer Aβ Induces Chromosome Mis‐segregation, Microtubule Defects, Receptor Mis‐localization, and Inhibition of Mitotic/Neuronal Kinesins: Implications for Neurogenesis and Plasticity in Neurodegenrative Diseases
  71. Alzheimer Aβ Peptide Induces Chromosome Mis-Segregation and Aneuploidy, Including Trisomy 21: Requirement for Tau and APP
  72. P1‐432: Alzheimer's mutant presenilin‐1 and amyloid precursor protein genes cause chromosome missegregation and aneuploidy through the action of Abeta peptide
  73. P3‐315: Inhibition of gamma‐secretase activity induces cell cycle defects and chromosome missegregation
  74. P4‐302: Lipoprotein‐induced chromosome missegregation in vitro and in vivo: Implications for cardiovascular and Alzheimer's disease
  75. Alzheimer's presenilin 1 causes chromosome missegregation and aneuploidy
  76. P3–227: Chromosome aneuploidy, including human trisomy 21 caused by Alzheimer's mutant presenilin 1/ Î3–secretase
  77. P4-293 The presenilins, chromosome missegregation, and Alzheimer's disease