Apolipoprotein E {Varepsilon}4 Does Not Modulate Amyloid-?-Associated Neurodegeneration in Preclinical Alzheimer Disease.

Apolipoprotein E {varepsilon}4 Does Not Modulate Amyloid-?-Associated Neurodegeneration in Preclinical Alzheimer Disease.

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AJNR Am J Neuroradiol. 2012 Sep 13;
Desikan RS, McEvoy LK, Holland D, Thompson WK, Brewer JB, Aisen PS, Andreassen OA, Hyman BT, Sperling RA, Dale AM,

BACKGROUND AND PURPOSE:Among cognitively healthy older individuals, the relationship among the 2 hallmark proteins of AD (A? and ? APOE ?4) and neurodegeneration is not well-understood. Here, we investigated the relationship between A?, p-?, and APOE ?4 on longitudinal brain atrophy in preclinical AD.MATERIALS AND METHODS:We examined 107 cognitively healthy older adults who underwent longitudinal MR imaging and baseline lumbar puncture. Within the same linear mixed-effects model, we concurrently investigated main and interactive effects between the APOE ?4 genotype and CSF A?(1-42), CSF p-? and CSF A?(1-42), and the APOE ?4 genotype and CSF p-? on entorhinal cortex atrophy rate. We also examined the relationship of APOE ?4, CSF p-?, and CSF A?(1-42) on the atrophy rate of other AD-vulnerable neuroanatomic regions.RESULTS:The full model with main and interactive effects demonstrated a significant interaction only between CSF p-? and CSF A?(1-42) on entorhinal cortex atrophy rate, indicating elevated atrophy with time in individuals with increased CSF p-? and decreased CSF A?(1-42). The APOE ?4 genotype was significantly and specifically associated with CSF A?(1-42). However, the interaction between the APOE ?4 genotype and either CSF A?(1-42) or CSF p-? on entorhinal cortex atrophy rate was not significant. We found similar results in other AD-vulnerable regions.CONCLUSIONS:On the basis of our findings and building on prior experimental evidence, we propose a model of the pathogenic cascade underlying preclinical AD in which APOE ?4 primarily influences the pathology of Alzheimer disease via A?-related mechanisms, and in turn, A?-associated neurodegeneration occurs only in the presence of p-?.
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Alcohol and cancer in the digestive tract.

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Nihon Shokakibyo Gakkai Zasshi. 2012; 109(9): 1518-25
Yokoyama A

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The Addiction Concept and Technology: Diagnosis, Metaphor, or Something Else? A Psychodynamic Point of View.

Filed under: Addiction Rehab

J Clin Psychol. 2012 Sep 13;
Essig T

Many today suffer from an imbalance between life and life on the screen. When extreme, such as excessive gaming, clinicians retreat to familiar explanations, such as “Internet addiction.” But the addiction concept is of limited value, limiting both research and treatment options. This article discusses an alternative. Pathological overuse is seen as a failed solution in which people become entrapped by technology’s promise of delivering that which only life can offer, such as the grand adventure simulated in World of Warcraft. A two-part treatment approach of such “simulation entrapment” is described in which both the original problem and the entrapment are treated, the former by traditional psychodynamic psychotherapy and the later by highlighting differences between the technologically mediated experience and traditional experiences of being bodies together. The case of a college student suffering from pathological shame with excessive gaming as the failed solution is offered as an illustration.
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Sex differences in novelty- and psychostimulant-induced behaviors of C57BL/6 mice.

Filed under: Addiction Rehab

Psychopharmacology (Berl). 2012 Sep 14;
Van Swearingen AE, Walker QD, Kuhn CM

RATIONALE: Women are more sensitive than men to psychostimulants and progress from initial use to drug addiction more quickly. The mouse has been an under-utilized model to study sex differences in psychostimulant action. Mice could serve as an ideal genetically tractable model for mechanistic studies into sex and hormone effects on psychostimulant behavior. OBJECTIVES: The objective of this study was to characterize psychostimulant effects in male and female mice with a combination of automated data collection and behavioral observation. METHODS: Male and female C57BL/6 mice (Charles River) were given a single dose or sequential ascending binge doses of D-amphetamine (AMPH) or cocaine (COC). Behavior was assessed in open field chambers using both automated photobeam interruptions and behavioral observations. Brain psychostimulant concentrations were determined at the time of maximum behavioral stimulation. RESULTS: Psychostimulants induced behavioral activation in mice including both increased locomotion as detected with an automated system and a sequence of behaviors progressing from stereotyped sniffing at low doses to patterned locomotion and rearing at high doses. Females exhibited more patterned locomotion and a shift towards higher behavior scores after either psychostimulant despite having lower AMPH and equivalent COC brain levels as males. CONCLUSIONS: Female C57BL/6 mice exhibit enhanced psychostimulant-induced behavior compared to males, similar to reports in rats. The combination of automated behavioral measures and behavioral observation was essential for verifying the existence of these differences. These results indicate the importance of testing both sexes when characterizing genetically manipulated mice to control for potential sex-specific effects.
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