Worldline CPT and massless supermultiplets

The action for a massless particle in 4D Minkowski space–time has a worldline-time reversing symmetry corresponding to CPT invariance of the quantum theory. The analogous symmetry of the $\mathscr{N}$-extended superparticle is shown to be anomalous when $\mathscr{N}$ is odd; in the supertwistor formalism this is because a CPT-violating worldline-Chern–Simons term is needed to preserve the chiral $\textbf{U(1)}$ gauge invariance. This accords with the fact that no massless $\mathscr{N}$=1 super-Poincaré irrep is CPT-self-conjugate. There is a CPT self-conjugate supermultiplet when $\mathscr{N}$ is even, but it has $\textbf{2}$$^{\mathscr{N}+1}$ states when $\frac{1}{2}$$\mathscr{N}$ is odd (e.g. the $\mathscr{N}$=2 hypermultiplet) in contrast to just $\textbf{2}$$^{\mathscr{N}}$ when $\frac{1}{2}$$\mathscr{N}$ is even (e.g. the $\mathscr{N}$=4 Maxwell supermultiplet). This is shown to follow from a Kramers degeneracy of the superparticle state space when $\frac{1}{2}$$\mathscr{N}$ is odd.A.S. Arvanitakis and P. K. Townsend acknowledge support from the UK Science and Technology Facilities Council (grant ST/L000385/1).A.S. Arvanitakis also acknowledges support from Clare Hall College, Cambridge, and from the Cambridge Trust

Pauli-Lubanski, supertwistors, and the superspinning particle

We present a novel construction of the super-Pauli-Lubanski pseudo-vector for 4D supersymmetry and show how it arises naturally from the spin-shell constraints in the supertwistor formulation of superparticle dynamics. We illustrate this result in the context of a simple classical action for a “superspinning particle” of superspin 1/2. We then use an Sl(2;K)-spinor formalism for K=ℝ,ℂ,ℍ to unify our 4D results with previous results for 3D and 6D

The Brodmann Area 39/40 of the Brain in Alzheimer’s, Mild Cognitive Impairment, and No Cognitive Impairment Subjects at Advanced Age Demonstrate Comparable Levels of Blood-Brain Barrier Breach

• Alzheimer’s disease (AD) is one of the most common form of dementia • Mild cognitive impairment (MCI), specifically amnestic subtype, more likely to progress to AD • Pathogenesis Theories: o Accumulation of amyloid-beta peptides and neurofibrillary tangles containing hyperphosphorylated neuronal tau protein o Blood Brain Barrier (BBB) dysfunction is associated with AD pathogenesis • Brodmann area 39/40: regions of parietal cortex are responsible for language, spatial cognition, memory retrieval, attention, phonological processing, and emotional processing • Hypothesis: An increased BBB permeability in Brodmann area 39/40 of AD and age-matched MCI and no cognitive impairment (NCI) subject

Diabetes Is Associated with Cerebrovascular but not Alzheimer\u27s Disease Neuropathology

INTRODUCTION: The relationship of diabetes to specific neuropathologic causes of dementia is incompletely understood. METHODS: We used logistic regression to evaluate the association between diabetes and infarcts, Braak neurofibrillary tangle stage, and neuritic plaque score in 2365 autopsied persons. In a subset of \u3e1300 persons with available cognitive data, we examined the association between diabetes and cognition using Poisson regression. RESULTS: Diabetes increased odds of brain infarcts (odds ratio [OR] = 1.57, P \u3c .0001), specifically lacunes (OR = 1.71, P \u3c .0001), but not Alzheimer\u27s disease neuropathology. Diabetes plus infarcts was associated with lower cognitive scores at end of life than infarcts or diabetes alone, and diabetes plus high level of Alzheimer\u27s neuropathologic changes was associated with lower mini-mental state examination scores than the pathology alone. DISCUSSION: This study supports the conclusions that diabetes increases the risk of cerebrovascular but not Alzheimer\u27s disease pathology, and at least some of diabetes\u27 relationship to cognitive impairment may be modified by neuropathology

Diabetes and the Risk of Developing Parkinson’s Disease in Denmark

Objective: Insulin contributes to normal brain function. Previous studies have suggested associations between midlife diabetes and neurodegenerative diseases, including Parkinson’s disease. Using Danish population registers, we investigated whether a history of diabetes or the use of antidiabetes drugs was associated with Parkinson’s disease. Research Design and Methods: From the nationwide Danish Hospital Register hospital records, we identified 1,931 patients with a first-time diagnosis of Parkinson’s disease between 2001 and 2006. We randomly selected 9,651 population control subjects from the Central Population Registry and density matched them by birth year and sex. Pharmacy records comprising all antidiabetes and anti-Parkinson drug prescriptions in Denmark were available. Odds ratios (ORs) were estimated by logistic regression models. Results: Having diabetes, as defined by one or more hospitalizations and/or outpatient visits for the condition, was associated with a 36% increased risk of developing Parkinson’s disease (OR 1.36 [95% CI 1.08–1.71]). Similarly, diabetes defined by the use of any antidiabetes medications was associated with a 35% increased Parkinson’s disease risk (1.35 [1.10–1.65]). When diabetes was defined as the use of oral antidiabetes medications, effect estimates were stronger in women (2.92 [1.34–6.36]), whereas when diabetes was defined as any antidiabetes drug prescription, patients with early-onset Parkinson’s disease were at highest risk (i.e., Parkinson’s disease diagnosed before the age of 60 years; 3.07 [1.65–5.70]). Conclusions: We found that a diagnosis of, or treatment received for, diabetes was significantly associated with an increased risk of developing Parkinson’s disease, especially younger-onset Parkinson’s disease. Our results suggest a common pathophysiologic pathway between the two diseases. Future studies should take age at Parkinson’s disease onset into account

Relationship Between Baseline Glycemic Control and Cognitive Function in Individuals With Type 2 Diabetes and Other Cardiovascular Risk Factors: The Action to Control Cardiovascular Risk in Diabetes-Memory in Diabetes (ACCORD-MIND) trial

OBJECTIVE—Diabetes is associated with cognitive decline and dementia. However, the relationship between the degree of hyperglycemia and cognitive status remains unclear. This was explored using baseline cognitive measures collected in the ongoing Memory in Diabetes (MIND) substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial

Intermediate Phenotypes Identify Divergent Pathways to Alzheimer's Disease

Background: Recent genetic studies have identified a growing number of loci with suggestive evidence of association with susceptibility to Alzheimer's disease (AD). However, little is known of the role of these candidate genes in influencing intermediate phenotypes associated with a diagnosis of AD, including cognitive decline or AD neuropathologic burden. Methods/Principal Findings: Thirty-two single nucleotide polymorphisms (SNPs) previously implicated in AD susceptibility were genotyped in 414 subjects with both annual clinical evaluation and completed brain autopsies from the Religious Orders Study and the Rush Memory and Aging Project. Regression analyses evaluated the relation of SNP genotypes to continuous measures of AD neuropathology and cognitive function proximate to death. A SNP in the zinc finger protein 224 gene (ZNF224, rs3746319) was associated with both global AD neuropathology (p = 0.009) and global cognition (p = 0.002); whereas, a SNP at the phosphoenolpyruvate carboxykinase locus (PCK1, rs8192708) was selectively associated with global cognition (p = 3.57×10−4). The association of ZNF224 with cognitive impairment was mediated by neurofibrillary tangles, whereas PCK1 largely influenced cognition independent of AD pathology, as well as Lewy bodies and infarcts. Conclusions/Significance: The findings support the association of several loci with AD, and suggest how intermediate phenotypes can enhance analysis of susceptibility loci in this complex genetic disorder