scholarly journals Discoverer of Alzheimer’s disease: Alois Alzheimer

2015 ◽  
Vol 6 (2) ◽  
pp. 56-61
Author(s):  
Masahito Watanabe
2020 ◽  
Vol 4 (1) ◽  
pp. 417-429
Author(s):  
Sushma Pradeep ◽  
Anisha S. Jain ◽  
Chandan Dharmashekara ◽  
Shashanka K. Prasad ◽  
Shiva Prasad Kollur ◽  
...  

Alzheimer’s disease (AD) was first described in 1907 and got its name after Alois Alzheimer, a German psychiatrist and neuropathologist. This disease starts slow, increasing gradually to worsen in the due course of time. AD is mainly characterized by the associated dementia, which is a decline of cognitive effects such as memory, praxis, and orientation. The dementia is further highlighted by the presence of psychological and behavioral symptoms. Additionally, AD is also associated with the multiple interconnected pathways linked neuropathological changes such as the formation of neurofibrillary tangles and amyloid-β plaques inside the brain. AD therapeutics have been of prime concern over the decades, resulting in the elucidation of promising therapeutic targets. The requirement of AD stage dependent optimized conditions has necessitated a combinatorial approach toward treatment. The priority in AD research has remained to develop disease-modifying and development-reducing drugs for treatment regimens followed during the early and later stages, respectively.


Author(s):  
Steven R. Sabat

Alzheimer’s disease (AD) was first identified by Alois Alzheimer in 1906 in his patient, Frau Auguste D. Dr. Alzheimer saw Frau D in 1901 and observed her rather striking symptoms that normally would have been described as “senile dementia.” It would have been called this...


2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Tomasz Jaworski ◽  
Sebastian Kügler ◽  
Fred Van Leuven

Patients suffering from Alzheimer's disease (AD) are typified and diagnosed postmortem by the combined accumulations of extracellular amyloid plaques and of intracellular tauopathy, consisting of neuropil treads and neurofibrillary tangles in the somata. Both hallmarks are inseparable and remain diagnostic as described by Alois Alzheimer more than a century ago. Nevertheless, these pathological features are largely abandoned as being the actual pathogenic or neurotoxic factors. The previous, almost exclusive experimental attention on amyloid has shifted over the last 10 years in two directions. Firstly, from the “concrete” deposits of amyloid plaques to less well-defined soluble or pseudosoluble oligomers of the amyloid peptides, ranging from dimers to dodecamers and even larger aggregates. A second shift in research focus is from amyloid to tauopathy, and to their mutual relation. The role of Tau in the pathogenesis and disease progression is appreciated as leading to synaptic and neuronal loss, causing cognitive deficits and dementia. Both trends are incorporated in a modified amyloid cascade hypothesis, briefly discussed in this paper that is mainly concerned with the second aspect, that is, protein Tau and its associated fundamental questions.


2015 ◽  
Vol 73 (2) ◽  
pp. 159-162 ◽  
Author(s):  
Eliasz Engelhardt ◽  
Marleide da Mota Gomes

Initially the trajectory of the historical forerunners and conceptions of senile dementia are briefly presented, being highlighted the name of Alois Alzheimer who provided clinical and neuropathological indicators to differentiate a group of patients with Senile dementia. Alzheimer's examination of Auguste D’s case, studied by him with Bielschowsky’s silver impregnation technique, permitted to identify a pathological marker, the intraneuronal neurofibrillary tangles, characterizing a new disease later named after him by Kraepelin – Alzheimer’s disease. Over the time this disorder became one of the most important degenerative dementing disease, reaching nowadays a status that may be considered as epidemic.


2021 ◽  
pp. 1-35
Author(s):  
Suélen Santos Alves ◽  
Rui Milton Patrício da Silva-Junior ◽  
Gabriel Servilha-Menezes ◽  
Jan Homolak ◽  
Melita Šalković-Petrišić ◽  
...  

Almost 115 years ago, Alois Alzheimer described Alzheimer’s disease (AD) for the first time. Since then, many hypotheses have been proposed. However, AD remains a severe health public problem. The current medical approaches for AD are limited to symptomatic interventions and the complexity of this disease has led to a failure rate of approximately 99.6%in AD clinical trials. In fact, no new drug has been approved for AD treatment since 2003. These failures indicate that we are failing in mimicking this disease in experimental models. Although most studies have focused on the amyloid cascade hypothesis of AD, the literature has made clear that AD is rather a multifactorial disorder. Therefore, the persistence in a single theory has resulted in lost opportunities. In this review, we aim to present the striking points of the long scientific path followed since the description of the first AD case and the main AD hypotheses discussed over the last decades. We also propose insulin resistance as a common link between many other hypotheses.


1997 ◽  
Vol 10 (4) ◽  
pp. 105-108 ◽  
Author(s):  
G. Macchi ◽  
C. Brahe ◽  
M. Pomponi

Three points of interest lie in considering how Alzheimer, and more significantly Perusini, struggled to throw light on the cause of this devastating disease. There is a stimulating possibility that Perusini believed presenile forms of Alzheimer’s disease described the same disease as senile forms. If so this would anticipate current opinion, and reveal Perusini to dissent from Kraepelin. In addition, Perusini may have understood the pathological relationship between neuritic plaques and vascular changes, once more foreseeing the modern view of Alzheimer’s disease. Finally, Perusini and Alzheimer disagreed with Jung's view concerning the relationship between neuropathology and clinical psychiatry. This point highlights the major change occurring at that time from classical neurology to the psychoanalytic era. In his last work (1911) Alzheimer quoted his Italian disciple many times, even speaking of ‘Perusini's cases’ (Perusinischen Fälle). This article is an attempt to change the eponym of Alzheimer’s disease into the Alzheimer-Perusini disease. This is a brief history of a master and his disciple, whose scientific lives were, by events, divided.


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