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The Genetics of Alzheimer Disease:
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
The evidence for the genetic independence of “Alzheimer’s disease” and “senile dementia” was highly circular. In the Sjogren et al. (1952) study no secondary “senile dementia” cases were reported among relatives of “Alzheimer’s disease” probands. However, as mentioned above, relatives over 70 were not evaluated for dementia. In the Larsson et al. (1963) study no presenile “Alzheimer’s” cases were reported in relatives of the “senile dementia” probands. Yet, secondary cases of “senile dementia” with symptomatic onset as early as at 52 years of age are described (Larsson et al., 1963, p. 64). This illustrates the bias which can be introduced into a generally rigorous study by preconceived assumptions about disease boundaries.
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Recent publications suggest that various etiological factors are responsible for senile dementia. The neuritic or senile plaques in Alzheimer’s disease consist of a dense core of extracellular amyloid surrounded by enlarged neurites containing degenerating mitochondria and lamellar lysosomes with increased hydrolase activity.554 Neurotransmitter substances,476,501 such as dopamine and norepinephrine, and the gabanergic system show significant losses with age, but there are no specific changes in Alzheimer dementia. Monoamine oxidase activity is increased in the brain in Alzheimer’s disease, and the levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid are decreased. Changes in the cholinergic system seem to be related, and choline acetyltransferase activity is reduced and acetylcholine increased in certain cortical areas in Alzheimer’s disease and related disorders.151,218,456,461,469,478,502
What is it about the nucleus?
Published in Brendan Curran, A Terrible Beauty is Born, 2020
However, in other, and thankfully rarer, cases the inherited dysfunction dominates the normal function; this means that the presence of one copy of the incorrect information is sufficient for the full disease to appear. Huntington’s chorea is just one example of this type of inherited disease. The inherited misinformation causes the production of an abnormal protein in the nerve cells in the brain. The abnormal protein interferes with the normal one so that, even though the cells are still producing lots of the normal protein, they cannot carry out their function and nerve degeneration becomes evident in late middle age. This manifests as early senile dementia with total mental and physical disability 10–20 years after the onset of the initial symptoms. As this is a dominant mutation, individuals who inherit just one copy develop the disease. But even more tragically, by the time they realise that they have the gene they have already had their own families and passed on their genes to the next generation. Regardless of the genetic information from the other parent, on average, half their offspring will by then have inherited the same dysfunction and will be destined to develop the disease (Figure 3.11 (b)).
Tadalafil ameliorates memory deficits, oxidative stress, endothelial dysfunction and neuropathological changes in rat model of hyperhomocysteinemia induced vascular dementia
Published in International Journal of Neuroscience, 2022
Chronic l-Methionine administration is well reported to produce HHcy induced endothelial dysfunction and related VaD [25,31,43,44]. HHcy has been associated with increased oxidative stress and is observed to decrease antioxidant enzyme activities and produce deleterious effects on endothelial cells causing endothelial cell damage [45–47]. However, oxidative stress has been considered as primary mechanism responsible for HHcy-related pathogenesis [48]. HHcy induced increase in oxidative stress has been suggested to play a major role in neurodegeneration [47,49]. Elevated homocysteine levels have also documented to enhance AChE activity in the central nervous system [50]. AChE enzyme activity is suggested as a marker of cognitive impairment which is responsible for the breakdown of acetylcholine [51]. According to the cholinergic hypothesis, memory impairment in senile dementia patients is due to the selective and irreversible deficiency in the cholinergic function of the brain [52]. It has been suggested that cholinergic neurotransmission not only affected in Alzheimer’s disease but also affected in VaD [53,54]. This is further supported by the results of present study indicating increase in brain AChE activity of hyperhomocysteinemic rats. Noticeable profound neuroinflammation as reflected by a rise in brain MPO activity and neutrophilic infiltration (observed in histological sections of brain slices) in the hyperhomocysteinemic rats is also supported by previous reports [47,55].
Synthesis and biological evaluation of 2-arylbenzofuran derivatives as potential anti-Alzheimer’s disease agents
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Yinling Yun, Yuhang Miao, Xiaoya Sun, Jie Sun, Xiaojing Wang
Alzheimer's disease (AD) is a type of progressive dementia caused by degeneration of the nervous system. It has a higher incidence in the elderly, so it is called senile dementia. Clinical manifestations are mainly memory impairment, cognitive dysfunction, mental symptoms, and behavioural abnormalities1. The two core pathological features of AD are amyloid plaques and neurofibrillary tangles2. AD features include progressive memory loss and severe cognitive decline. AD is a typical multifactorial disease, and its pathogenesis involves abnormalities in the structure and function of multiple systems3. Therefore, single-target drugs often do not work well. Design and develop multi-target drugs so that one drug can specifically bind to multiple targets to ensure clinical effectiveness while reducing toxicity.
Traditional Ayurvedic and herbal remedies for Alzheimer’s disease: from bench to bedside
Published in Expert Review of Neurotherapeutics, 2019
Rohit Sharma, Kamil Kuca, Eugenie Nepovimova, Atul Kabra, MM Rao, PK Prajapati
As per Ayurveda, Tridosha and Triguna are the bioenergies/life forces which regulate physiological and psychological functions of human body. Disruptions in Tridosha and Triguna will impact the Indriya (cognitive and motor organs), Manas (psyche), and Buddhi (intellect) in negative manner, consequently, it will affect the memory negatively [50,51]. AD cannot be exactly equated to any clinical condition as described in Ayurveda. But in Ayurvedic, classic Smritinasha (amnesia) is mentioned among the prodromal symptom of Jara (aging). In Jaravastha (old age), which starts from 60 years of age, the functions of memory and other mental faculties gradually deteriorate naturally. Further, Smritibhramsha (disturbed memory) is described as a symptom where Smriti (memory) is vitiated by Rajas (passion) and Tamas (obscurity). Thus, senile dementia can be interpreted as Jarajanya Smritibhramsha according to Ayurvedic principles [52]. Ayurveda considers nervous system disorders under Vata Vyadhi concept, which are considered critical to treat because of their severity and cured by rigorous panchakarma (biopurification) and palliative medicines by skilled physician [53]. Diagnosis and exact symptomatic manifestation of neurodegenerative disorders requires substantial clinical acumen. Ayurvedic approach can be used in AD’s management through (1) creating an equilibrium of Tridosha and Triguna, essential for maintaining the cognitive functions, and (2) promoting healthy aging via Rasayana drugs or psychotherapies.