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An air of scandal has always surrounded German idealism. A defender of common sense might already be scandalised by the extraordinary complexity of many German idealists’ writings. If their language is difficult, it is partly because the era of idealism belongs to the era of the discovery of the philosophical resources of the German language: the philosopher finding ideas also had to be a writer finding the words to express them. What is more, the idealists seem to abandon “common sense” because they skip the problems of the traditional school logic and seek, instead, a logic of subjectivity and of being. These logics cannot be reduced to the operations of the “understanding” and constitute what the idealists named “reason”.

Analytical philosophy of mind is currently engaged in a renewed and intensified debate about such issues as subjectivity, phenomenal consciousness, and the nature of selfhood.While it is undeniable that its discussion of these topics has reached a high level of complexity and sophistication, it is however, a discussion that has also remained rather inward looking. Apart from some occasional references to historical figures such as Locke or Kant or James, it has largely been a discussion for and among analytical philosophers. There has been a lack of any real interest in the parallel discussions to be found on the Continent, even though there is a long and rich tradition for discussing and analyzing the very same problems in Austrian, German, and French philosophy.

Consciousness occupies a central place in contemporary Anglophone philosophy of mind. One reason why this is so – and we shall expand upon this later – is that consciousness poses a for naturalist theories of mind. Most Anglophone philosophers of mind are committed to the view that social, linguistic and psychological facts supervene upon and are determined by facts about the objective, non-mental, causal world, a world studied and explained by physics, chemistry, biology and other “natural” sciences. Whilst most philosophers agree that consciousness poses a problem for this naturalistic conception of the world, there is considerable disagreement about what consciousness is. This is, perhaps, not surprising. It has long been recognised that ‘consciousness’ is an ambiguous, polysemic notion.

Pedigrees with familial Alzheimer's disease (FAD), caused by mutations in either the amyloid precursor protein (APP) or the presenilin 1 (PS1) or presenilin 2 (PS2) genes, show considerable phenotypic variability. Monogenic diseases typically exhibit variations in biological features, such as age of onset, severity, and multiple clinical and cellular phenotypes. This variation can be due to specific alleles of the disease gene, environmental effects, or modifier genes.

Spastic paraparesis (SP), or progressive spasticity of the lower limbs, is frequently hereditary, with over 20 loci being identified for uncomplicated (paraparesis alone) and complicated (paraparesis and other neurological features) disease subtypes. Moreover, over 10 different genes have been identified with mutations that lead to SP. While dementia is a common feature of complicated SP, a reciprocal observation has also been made since the earliest clinical reports of FAD: namely, that a number of AD families have been reported in which some individuals have SP. In 1997, the key observation was made that PS1 mutations were associated with the presence of SP, suggesting that there was a complex relationship between SP and AD. In addition, in 1998, it was also shown that PS1 AD/SP pedigrees frequently have variant, large, non-cored plaques without neuritic dystrophy, named cotton wool plaques (CWP). The PS1 mutations associated with CWP secrete unusually high levels of the amyloid β 42 peptide, suggesting a molecular basis for the formation of this distinctive plaque type.

The SP phenotype in PS1 pedigrees appears to be associated in some cases with a delayed onset of dementia, compared with affected individuals who present with dementia only. Some individuals who present with SP have remained dementia-free for up to 10 years. Variations seen in neuropathology and neurological symptoms in PS1 FAD suggest that modifier genes may underlie this phenotypic heterogeneity. As PS1 mutations are almost always associated with a particularly aggressive form of presenile dementia, these findings suggest the existence of a protective factor in some individuals with SP.