Alzheimer's Disease: My Point of View (Editor's Note)

2001 ◽  
Vol 17 (2) ◽  
pp. 269-270 ◽  
Author(s):  
Illana Gozes
2018 ◽  
Vol 19 (9) ◽  
pp. 2603 ◽  
Author(s):  
Claudia Campanella ◽  
Andrea Pace ◽  
Celeste Caruso Bavisotto ◽  
Paola Marzullo ◽  
Antonella Marino Gammazza ◽  
...  

Among diseases whose cure is still far from being discovered, Alzheimer’s disease (AD) has been recognized as a crucial medical and social problem. A major issue in AD research is represented by the complexity of involved biochemical pathways, including the nature of protein misfolding, which results in the production of toxic species. Considering the involvement of (mis)folding processes in AD aetiology, targeting molecular chaperones represents a promising therapeutic perspective. This review analyses the connection between AD and molecular chaperones, with particular attention toward the most important heat shock proteins (HSPs) as representative components of the human chaperome: Hsp60, Hsp70 and Hsp90. The role of these proteins in AD is highlighted from a biological point of view. Pharmacological targeting of such HSPs with inhibitors or regulators is also discussed.


Author(s):  
Sandro Sorbi ◽  
Camilla Ferrari

The history of Alzheimer's disease (AD) started in 1907, but we needed to wait until the end of the century to identify the component of pathological hallmarks, genetic subtypes and to formulate the first pathogenic hypothesis. Thanks to biomarkers and new technologies, the concept of AD then rapidly changed from a static view of an amnestic dementia of the presenium to a biological entity that could be clinically manifested as normal cognition or dementia of different types. What is clearly emerging from studies is that AD is heterogeneous in each aspect, such as amyloid composition, tau distribution, relation between amyloid and tau, clinical symptoms, genetic background, and thus it is probably impossible to explain AD with a single pathological process. The scientific approach to AD suffers from chronological mismatches between clinical, pathological and technological data, causing difficulty in conceiving diagnostic gold standards and in creating models for drug discovery and screening. A recent mathematical computer-based approach offers the opportunity to study AD in real life and to provide a new point of view and the final missing pieces of the AD puzzle.


Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1267 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Md. Tanvir Kabir ◽  
Kamal Niaz ◽  
Philippe Jeandet ◽  
Christophe Clément ◽  
...  

Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer’s pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis.


2008 ◽  
Vol 9 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Lorenzo Pia ◽  
Paul M. Conway

AbstractNeurological patients can be entirely unaware of their disease; this phenomenon is called anosognosia and it has been shown in different sensory-motor and cognitive domains. Lack of awareness has been investigated in Alzheimer's disease (AD) and within different domains of it. In the present article we review the literature on anosognosia for AD that had been indexed on the Medline database until the end of 2004. Historical introduction to the subject is followed by a brief description of the anatomy and clinical characteristics of AD. An analysis of a number of studies that focus on the relationship between anosognosia and AD then follows. This review shows that anosognosia is typical in AD, compared with other types of dementia, and it is a distinctive feature in the most severe cases and particularly in the beginning phases of illness. From an anatomical point of view, anosognosia seems to be strictly connected to frontal lobe areas; in fact, patients with anosognosia and AD show a reduction of cerebral haematic flow in the frontal regions, as well as deficits of executive functions and extrapyramidal signs. Interestingly, co-occurring depression could be interpreted as an adaptive behavior to counter the effects of perceived loss of cognitive abilities. Finally, self-awareness in AD could have some common mechanisms with auto-monitoring in schizophrenia.


2011 ◽  
Vol 7 ◽  
pp. S304-S304
Author(s):  
Melissa Murray ◽  
Neill Graff-Radford ◽  
Dennis Dickson

2021 ◽  
Vol 17 (S9) ◽  
Author(s):  
Lois Ottenhoff ◽  
Everard G.B. Vijverberg ◽  
Leonie N.C. Visser ◽  
Merike Verrijp ◽  
Niels D. Prins ◽  
...  

2018 ◽  
Vol 67 (4) ◽  
pp. 451-463
Author(s):  
Stefano Fuselli

Il morbo di Alzheimer è una patologia i cui effetti non sono dirompenti solo sul piano pratico, per i pazienti e i loro familiari o per il sistema socio-assistenziale, ma anche sul piano concettuale. Esso infatti mette a dura prova le correnti nozioni di identità e autonomia del soggetto, con notevoli conseguenze, prima ancora che sul piano pratico, sul piano teorico. Muovendo dal dibattito bioetico attuale, questo contributo intende portare allo scoperto quanto nel dramma dell’Alzheimer si manifesta circa la nozione di identità e di autonomia. La prospettiva prescelta non è pratica ma è teoretica, volta cioè non tanto al da-farsi ma al da-guardarsi. ---------- The effects of Alzheimer’s Disease are disruptive on a practical level for patients and their families as well as for the healthcare system. They are also disruptive on a conceptual level, because they challenge the current notions of identity and autonomy of the subject. The consequences are relevant first and foremost from a theoretical point of view rather than from a practical one. By considering the present debate in bioethics, this contribution aims to shed light on what AD can reveal about the notions of identity and autonomy. The perspective is a theoretical rather than a practical one, because it focuses on what has to be looked at rather than on what has to be done.


Alzheimer’s disease and vascular dementia are acknowledged as the two most common types of dementia. Each of these dementia syndromes are associated with prodromal clinical syndromes, often referred to as mild cognitive impairment. Recent research has demonstrated considerable heterogeneity regarding the underlying neuropathology associated with these dementia syndromes and their prodromal disorders. Thus, it is often difficult to understand how or what underlying biological substrate is actually responsible for the alterations in neurocognition and behaviour as seen in clinical evaluations. This inherent neuropsychological and neuropathology heterogeneity calls into question current paradigms used for diagnosis and clinical trials designed to treat these disorders. This volume summarizes our current understanding regarding the inherent clinical, neuropathological, and biological heterogeneity in Alzheimer’s disease, vascular dementia, and mild cognitive impairment and suggests that these disorders are best viewed as existing along a continuum rather than treated as separate and distinct clinical syndromes. In this book, we put forth the point of view that dementia such as Alzheimer’s disease and vascular dementia; and subtle pre-dementia syndromes such as mild cognitive impairment are best viewed as existing along a continuum rather than distinct and separate disorders.


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