J Neural Transm (2006) 113: 1595
DOI 10.1007/s00702-006-0590-7
Editorial – 100 years of Alzheimer’s disease
This issue is devoted to Alois Alzheimer whose work and
ideas formed the basis for our present understanding of
the disorder carrying his name. Alzheimer detected two
samples of patients of different ages whose brains exhibited
the same morphology associated with identical clinical
symptoms: age-dependent senile dementia and presenile
dementia. Additionally, this issue is devoted to Emil
Kraepelin who proposed the term ‘‘Alzheimer disease’’
and who first discussed that presenile dementia may be a
peculiar disease independent of age. This differentiation
represents present knowledge. The majority of people suf-
fering from dementia in old age may be classified as sporad-
ic Alzheimer disease, the causation(s) of which is (are) as
yet unknown. However, it is discussed for longer that dif-
ferent age-related changes may considerably contribute to
the onset of the disease: susceptible genes, hormones such
as insulin and cortisol, acute phase proteins, metabolic ab-
normalities at the cellular and molecular levels such as in
glucose=energy formation, neurotransmitter changes, free
radical formation, consequently enabling and facilitating
the formation of the morphological hallmark b-amyloid
containing neuritic plaques and hyperphosphorylated tau
protein containing neurofibrillary tangels. In contrast, the
formerly termed presenile dementia may be the hereditary
form of the disease. This, however, is very rare, and the
abnormal formation of b-amyloid from the beginning due
to three mutated genes may be its origin.
To adhere to the term ‘‘Alzheimer disease’’, this di-
agnosis comprises the age-dependent, sporadic type of
Alzheimer disease, whereas the hereditary early-onset type
represents an exceptional form different in nosology.
This issue deals with different aspects of sporadic
Alzheimer disease underlying the origin of cell loss and
the formation of the hallmarks neuritic plaques and neu-
rofibrillary tangle