**3. Properties**

The analytical techniques based on neutron activation are classified according to energy of incoming neutrons, elastic and inelastic neutron scattering, and neutron capture reactions as well as its combination such as thermal NAA (TNAA), epithermal NAA (ENAA), prompt gamma NAA (PGNAA), fast NAA (FNAA), and 14-MeV INAA a form of FNAA based on reactions with 14-MeV neutrons that are produced by neutron generators. These techniques have big application potential since they could provide data about large number of elements simultaneously. **Figure 1** presents more than 65 elements that may be analyzed using neutron activation analysis method. For most elements, NAA is an extremely sensitive method for analysis. The potential benefits of NAA include the multielement capability and the fact that non-destructive analyses can be performed.

The k0

of the k0

mandate of the k0

neutron activation analysis, k0

users to contact members of the k0

and improvement of the recommended k0

Subcommittee, and the maintenance of the k0

and application of the k0

**4.2. International k0**

cepts and procedures of the k0

www.kayzero.com/k0

of the laureates of George de Hevesy award during the period 1968–2018 [10].

use in numerous laboratories all over the world [19–29]. The official k0

**Figure 2.** *George de Hevesy* (1885–1966) who received the Nobel Prize for Chemistry in 1943.

naaorg/k0

**-Users Workshops**

of neutron activation analysis (**Table 2**). The k0

naa/k0

method and all associated events and database [24].

method include the coordination of the k0

*George de Hevesy* (1885–1966) received the Nobel Prize for Chemistry in 1943 for his work on the use of isotopes as tracers in the study of chemical processes. The Hevesy Medal as illustrated in **Figure 2** is the premier international award of excellence honoring outstanding achievements in radioanalytical and nuclear chemistry as illustrated. **Table 1** presents the list

The development of k0-NAA method is one of the most remarkable advances in the history

accurate models of the neutron activation, radionuclide decay, and gamma-ray detection processes. During the period 1970–1980, Prof F. De Corte (University of Gent, Belgium) and Dr. A. Simonits (KFKI-AEKI, Budapest, Hungary) and many co-workers developed the con-

5

Overview of Neutron Activation Analysis http://dx.doi.org/10.5772/intechopen.85461

website to give information and to allow k0


**1. Introduction**

[134] Jack CR, Knopman DS, Jagust WJ, et al. Hypothetical model of dynamic biomarkers of

[135] Storandt M, Head D, Fagan AM, Holtzman DM, Morris JC. Toward a multifactorial

[136] Rowe CC, Ellisa KA, Rimajova M, Bourgeat P et al. Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Neurobiol Aging

[137] Kohannim O, HUa X, Hibar DP, Lee S, Chou U, Toga AW et al. Boosting power for clinical trials using classifiers based on multiple biomarkers. Neurobiol Aging 2010;

[138] Lorenzi M, Donohue M, Paternico D, Scarpazza C et al. Enrichment through biomarkers in clinical trials of Alzheimer's drugs in patients with mild cognitive impairment.

[139] van Rossum IA, Vos S, Handels R, Visser PJ. Biomarkers as Predictors for Conversion from Mild Cognitive Impairment to Alzheimer-Type Dementia: Implications for Trial

[140] Yu P, Dean RA, Hall SD, Qi Y et al. Enriching Amnestic Mild Cognitive Impairment Populations for Clinical Trials: Optimal Combination of Biomarkers to Predict Con‐

[141] Lopez OL, Schqam E, Cummings J, Gautheir S, Jones R et al. Predicting cognitive decline in Alzheimer's diseae: An integrated analysis. Alz Dement 2010; 6:431-9.

version to Dementia. J Alz Dis; doi 10.3233/JAD-2012-120832.

the Alzheimer's pathological cascade. Lancet Neurol 2010; 9:119-28

model of Alzheimer disease. Neurobiol Aging 2012; 33:2262-71.

2010; 31:1275-83.

Neurobiol Aging 2010; 31:1443-51.

Design. J Alz Dis 2010; 20:881-91.

31:1429-42.

408 Understanding Alzheimer's Disease

*"I have lost myself"*

*- Auguste Deter, the first patient diagnosed with Alzheimer's Disease, 1906*

**Identification of Alzheimer's Disease** Alois Alzheimer was a German neuropathologist and among the first to identify and describe the hallmarks of what is known today as Alzheimer's disease (AD). In November of 1901, Dr. Alzheimer was presented with 51 year-old Auguste Deter who was suffering from mental incompetence, aphasia, disorientation, paranoia, and unprovoked bursts of anger. Deter's emotional and mental devastation became evident when she confided to Dr. Alzheimer "I have lost myself."

Symptoms similar to Deter's had been observed in patients for years and were considered a natural part of aging. However, it was unusual for such a pointed disease state to occur in someone so young. Over the next four and half years, Deter became increasingly demented, until her death at the age of 55. Upon examination of Deter's brain, Dr. Alzheimer found microscopic strands of protein which he described as "tangled bundles of fibrils" (neurofi‐ brillary tangles) in addition to "miliary foci" (amyloid plaques). In 1906, at the 37th Conference of South-West German Psychiatrists in Tübingen, Alois Alzheimer presented Deter's case as, "a peculiar disease of the cerebral cortex."

To this day both the cause of and treatment for AD remain a mystery. AD is a multifaceted disease of great complexity, however, over 100 years of research has provided clues to its mechanisms. Of particular recent interest is the emerging realization that another rapidly growing disease, type 2 diabetes mellitus (T2DM), is linked to development of AD [1].

This chapter examines the current state of knowledge regarding the association of T2DM to vascular changes in the brain and the implications these changes have in AD development.

© 2013 Aulston et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Other factors that contribute to AD such as insulin resistance and accumulation of the neurotoxic peptide amyloid beta (Aβ) are also examined. It's likely that no central cause of AD exists but rather, the disease represents a breakdown of several critical components involved in the general health and function of the brain.

**Vascular complications associated with type 2 diabetes** It is estimated that approximately 200 million people worldwide have diabetes and by 2025 the number is expected to increase to 333 million [22]. Epidemiological studies have indicated that patients with T2DM have a greater incidence of cardiovascular disease, cerebrovascular disease (CVD), hypertension and renal disease relative to the general population [8, 9]. In addition, a large number of populationbased studies have identified diabetes as a risk factor for dementia [23-25], primarily as a result of CVD [26, 27]. At only 3% of body weight, the brain uses ~20% of the body's oxygen and ~25% of the body's blood glucose [28, 29], demonstrating that it is by far the most metabolically active organ. This oxygen and glucose consumption is constantly required, since brain neurons are obligate aerobic cells and have no other source of energy. The majority of this energy is used to maintain cellular ionic homeostasis, and thus when cerebral blood flow (CBF) ceases, brain function ends within seconds and damage to neurons occurs within minutes [30].

Alzheimer's Disease and Diabetes http://dx.doi.org/10.5772/54913 411

The vascular complications associated with diabetes can be divided into two classes based on the vascular etiology of their pathology: macrovascular (hypertension, coronary artery disease, atherosclerosis, stroke) and microvascular (neuropathy, retinopathy, nephropathy). Macro‐ vascular complications are those that affect the larger (non-capillary) blood vessels. Statistics show that diabetes increases the risk of stroke and atherosclerosis [31]. Atherosclerosis accounts for 70% of morbidity associated with T2DM [32], while other studies have shown an association between the degree of hyperglycemia and increased risk of myocardial infarction and stroke [33-36]. While macrovascular complications themselves represent important pathological consequences of T2DM, they have also been shown to provide the etiological link

**Link between type 2 diabetes and Alzheimer's disease** AD is an age-related disorder characterized by progressive cognitive decline and dementia. An estimated 5.3 million people in the United States are currently affected and represents the sixth-leading cause of death. Significant evidence has been provided that links T2DM to AD. For example, a comprehensive meta-analysis showed that the aggregate relative risk of AD for people with diabetes was 1.5 (95%-CI 1.2 to 1.8) [37]. Studies have shown that T2DM, impaired fasting glucose and increased islet amyloid deposition are more common in patients with Alzheimer's disease than in control subjects [38, 39]. Unsurprisingly, insulin signaling provides an important mechanistic link

Ischemic CVD caused by T2DM is positively associated with AD through shared pathological mechanisms such as hyperinsulinemia, impaired insulin signaling, oxidative stress, inflam‐ matory mechanisms and advanced glycation end-products (AGEs) [40]. Defective insulin signaling is associated with decreased cognitive ability and development of dementa, includ‐ ing AD [41], rendering signaling neurons more vulnerable to metabolic stress and accelerating neuronal dysfunction [42]. In vitro insulin-stimulated Akt phosphorylation is decreased in hyperinsulinemic conditions in cortical neurons [43]. Finally, all forms of amyloid beta (Aβ) (monomers, oligomers and Aβ-derived diffusible ligands (ADDLs)) can inhibit insulin

signaling by directly binding to the insulin receptor and inhibit insulin signaling [44].

**Mechanisms of macrovascular complications of diabetes** A central pathological mechanism in diabetic-related macrovascular disease is atherosclerosis, which leads to the hardening of

between T2DM and the development of Alzheimer's disease.

between T2DM and AD.

**Epidemiology of AD and T2DM** AD is the most common form of dementia [2] and remains incurable. While the cause of AD remains unknown, several risk factors have been identified that may provide insight into the fundamentals of AD pathogenesis.

T2DM is a known risk factor for AD [1] suggesting that insulin signaling abnormalities play a central role in AD pathology. Moreover, AD brains show decreased insulin levels, decreased activity of insulin receptors and signs of compensatory mechanisms such as increased insulin receptor density [3] indicating AD as "type 3 diabetes" [4, 5].

Loss of insulin signaling in diabetes can occur by either type 1 or type 2 processes. Type 1 diabetes mellitus (T1DM) is characterized as an autoimmune disease that results in the destruction of insulin producing β cells found in the pancreas. In contrast, T2DM is a state of insulin resistance in which insulin levels are normal or elevated but tissues are unresponsive to its effects. While both T1DM and T2DM can lead to cognitive deficits, T2DM poses a greater risk for AD development [6, 7] and as a result the parallels between T2DM and AD are studied more vigorously than T1DM associations. Therefore, the majority of information presented here pertains to type 2 diabetic pathologies.

In addition to insulin resistance, T2DM is associated with the development of vascular dysfunction in the brain [8, 9]. T2DM is a risk factor for microvascular complications as well as macrovascular defects [10] such as stroke [11]. Vascular abnormalities are strongly associ‐ ated with AD [12-16] implying further involvement of T2DM in disease onset.


**4. Conclusion**

used signs, indigenous weather forecasters can hazard misinterpretation. Hence, indigenous experts are unable to update their science in view of changed environmental and ecological conditions that directly impact the stimulus-reaction pattern displayed for ages. On the other hand, it is very difficult to excuse the ever dwindling efficiency of astrology-based forecasts since the movement of celestial bodies and their constellations hardly change over brief span of time. Two possible explanations may be forwarded. First, in the past, the occurrence of drought had a more or less regular pattern, recurring once in a decade. Working on understanding of the observed regular pattern of the occurrence of drought might have deluded indigenous astrologists as having been correct in their forecasts. In recent years, however, global weather change has considerably distorted the old pattern of climate conditions with the effect that the forecasts of astrologists would not match with the reality. This means that from the outset, the knowledge claims of astrologists are found on pseudo-epistemology. This seems to be the reason for the failure/unwillingness of astrologist to explain why they read

and interpret certain celestial alignments and constellations the way they do.

**3.6. Socioeconomic preparations in view of expected drought**

human civilization attests.

154 Indigenous People

Secondly, the younger generation seems to have lacked fascination with the wisdom of forefathers, thereby undermining curiosity to learn the difficult technique of weather forecasting. As pointed out above, the expansion of alien ideas through education and monotheistic religions would stand negatively to the prestige and acceptability of indigenous experts, thereby inducing them to shy away from their indigenous practice. The bottom line is that people are no longer ready to seriously subscribe to indigenous forecasts. It would be impudent to argue that people should abandon their tradition at a time when science cannot provide a viable substitute. The best suggestion seems that indigenous experts should disclose their secrets to scientists so that a hybrid of climate forecasting system could be designed in ways that would make consideration of new biologist and animist signs as valid indicators of future weather phenomenon. It should not be difficult for indigenous experts to disclose their secrets as it would not represent any material lose since they are not paid for their service in the first place. They should be convinced that harmonious blend of indigenous and innovation has been inalienable prerequisites for survival and prosperity, as the history of

Indigenous knowledge-based weather forecasting is the main source of weather information in Borana where access to modern weather information is limited. In Borana weather forecast is disseminated using well-organized cultural network. In view of drought forecast, herders take different preparations: they stop sawing crops for a while, strengthening enclosure through community bylaw, saving water and grass, preparing livestock medicine, storing hay, migrating with animals, destocking, and changing schedules of social and cultural festivities such as wedding. In Borana, indigenous weather forecasting is becoming unreliable, and herders were victimized by incorrect prediction. However, still herders prefer indigenous weather forecast information than modern forecast information. They were reluctant to heed development agents' advice about modern weather information. This shows that integration of herders' skill and knowledge with

the modern weather forecasting system and dissemination should be a topical issue.

Migrating with animals where water and pasture are available areas is widely practiced as a coping strategy to drought. However, in the event of seasonal migration caused by drought, The study shows that indigenous weather forecasting has its own merits and demerits. The main quality of indigenous weather forecasting lies in the longer temporal horizon it covers. Whereas modern meteorology could offer a probable weather scenario for weeks and a few months, traditional weather forecasting offers probable weather scenario for a longer period. The degree of accuracy of traditional weather forecasting varies depending on the quality of experts, the base of the forecasting, and the complexities caused by climate change. Currently, the acceptance of indigenous weather forecasting is decreasing because of cultural assault perpetrated by the expansion of Islam, Christianity, and modern education. The intrinsic merits of traditional weather forecasting have not been a subject of serious scientific scrutiny. It is a high time that the tenets of indigenous weather forecasting be assessed scientifically and be integrated into the modern science before they vanish. This could improve the performance of weather forecasting for a better climate change adaptation.