In the 8th edition (1910) of "Psychiatric: Ein Lehrbuch fur Studirende und Arzte", Kraepelin stated that a "particular group of cases with extremely serious cell alterations" were discussed by Alzheimer. Those changes were: "Excessively numerous plaques, dying of almost one-third of the cortical cells, and peculiar, deeply stained bundles of neurofibrils in place of them". According to Kraepelin, these changes: "represent the most serious forms of senile dementia". Kraepeline mentioned "Alzheimer's Disease" for the first time when he stated that: "The clinical interpretation of this Alzheimer's Disease is still unclear". Since that time, there were doubts about the diagnosis of Auguste Deter's illness (the first case that Alzheimer introduced in 1906), and why did Kraepelin name this condition as Alzheimer's Disease. Now after 99 years there seem to be reliable answers to these questions. Description of Auguste Deter's Dementia by Alzheimer in 1907, and then By Perusini in 1909, indicated the senile plaques and neurofibrillary tangles. Besides, Perusini restudied the brain of this case and found no significant signs of arteriosclerosis. In 1998, scientists at the Max Planck Institue of Neurobiology, Martinsried, Germany, and at the University of Munich, rediscovered brain sections of the first reported case of Alzheimer's disease. Examination of these tissue sections showed a large number of neurofibrillary tangles and amyloid plaques. So, this case represents a typical example of Alzheimer's disease according to today's standards. It is interesting, too, that in 1997 Dr. Graeber and his colleagues in Max Planck Institute of Psychiatry, Department of Neuromorphology, Martinsried, Germany, had identified well-preserved histological brain sections of Alzheimer's second case, known as Johann F. Examination of the patient's brain revealed numerous amyloid plaques, but no neurofibrillary tangles in the cerebral cortex, corresponding to a less common form of Alzheimer's disease which may be referred to as "Plaque only". The researchers in Max Panck Institute performed mutational screening of exon 17 of the amyloid precursor protein gene and genotyping for apolipoprotein E alleles. The patient was shown to be homozygous for aplipoprotein E allele epsilon 3 and lacked APP mutations at codons 692, 693, 713 and 717. With regard to the brain sections of Auguste D., genotyping for the apolipoprotein E epsilon 4 allele revealed absence of this Alzheimer's disease "risk factor" but at the same time demonstrated that mutation analysis of the more than 90 year old brain tissue was still feasible. In the hundredth anniversary of Dr. Alzheimer's historical exploration, his findings are newly confirmed.