Predicting Alzheimer's Disease Progression by Combining Multiple Measures

Alzheimer's disease (AD) is a degenerative brain ailment that affects millions worldwide. It is the most common form of dementia. Patients with an early diagnosis of Alzheimer's disease have a strong chance of preventing additional brain damage by halting nerve cell death. At the same time, it begins to progress several years before any symptoms appear. The variety of data is the biggest problem encountered during diagnosis. Neurological examination, brain imaging, and often asked questions from his connected closed relatives are the three forms of data that a neurologist or geriatrics employs to diagnose patients. One of the biggest questions which need answering is the choice of a convenient feature. The main objective of this paper is to help neurologists or geriatricians diagnose patient conditions. It proposes a new hybrid model for features extracted from medical data. It discusses AD's early diagnosis and progression for all features considered in the diagnosis and their complex interactions. It proves to have the best accuracy when compared with the state-ofthe-art algorithm. Also, it proves to be more accurate against some recent research ideas. It got 95% in all cases, considering this work focused more on increasing the number of instances in comparison.

What causes selective nerve cell damage?

This chapter describes some of the work which has been undertaken to understand the cause of the selective nerve cell death which occurs in Huntington’s disease (HD). It has long been recognized that the change in the gene results in the protein product doing something which it should not: this is called a gain of function mutation. Despite the identification of the gene nearly 30 years ago a coherent story of the cause of the neurodegeneration has not been established. The chapter describes some of the animal models which have been developed and also the neuronal inclusions or aggregates which develop in cells.

High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

Plejotropowe działanie melatoniny

Melatonin is a hormone synthesized mainly by the pineal gland. Its precursor is the exogenous amino acid L-tryptophan. The basic function of this hormone is the regulation of circadian and seasonal rhythms. As an amphiphilic molecule, melatonin can easily cross biological barriers, which is why its effects can be exerted through a variety of mechanisms. Both in experimental and clinical studies, the cardioprotective effect of melatonin has been demonstrated. Melatonin also plays a role in the regulation of the immune response. In addition, it is particularly effective in inactivating hydroxyl radicals, including the most reactive oxygen radical. Melatonin can inhibit the division of tumor cells by affecting the release of other hormones and substances involved in the process of carcinogenesis. It also limits the process of nerve cell death and adverse changes in the nervous system associated with the etiopathogenesis of Alzheimer’s disease. Melatonin is on the list of OTC preparations (over the counter), medicines available at the pharmacy without a prescription. This paper presents the biosynthesis of melatonin and its metabolism and discusses its physiological and clinical significance in the human body.