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Introduction and Development: Over the next 50 years, the proportion of the population over the age of 65 will increase dramatically, and the number of individuals with neurodegenerative dementias such as Alzheimer's disease will rise, as well. Current pharmacological and non-pharmacological treatment strategies have focused on the symptomatic phases of Alzheimer's disease, but with the ability to identify the disease earlier in its clinical course comes an increased under-standing of the factors that alter the risk of expressing the clinical syndrome., Conclusions: Neuroimaging studies are now revealing that many of the conditions that normally afflict individuals as they become older also have effects on the structural integrity of the brain. Successful management of these conditions, especially if combined with other therapeutic interventions, could extend the dementia-free time and decrease the burden to the patient, family, and to society.

Alzheimer s disease (AD) is an insidious, and progressive disorder of the nervous system that typically occurs after age 65, with incidence rising with chronological age. The disorder is characterized by a pronounced memory loss, due to neuropathological changes in the mesial temporal lobes; as the pathology spreads throughout the cerebral cortex. However, it is still unknown why some areas are more affected than others, with the subsequent clinical heterogeneity (or phenotypes), and variability in the clinical course. The most salient neurobehavioral syndromes that can affect the clinical course are extrapyramidal signs, as well as a wide variety of psychiatric syndromes (e.g., psychotic symptoms, depression, aggression). Similarly, medication use (e.g., antipsychotics, sedatives) have shown to have a detrimental effect in the course of the disease. Current palliative treatments for AD may alter the natural history of the disease by extending the time that affected patients may live at home.

Objective: To review the experience of the last twenty years in the treatment of Alzheimer s disease (AD)., Methods: Literature review., Results: The neuropathological bases of AD are centered on two important pathophysiological mechanisms: 1) Structural damage (e.g., senile plaques, neurofibrillary tangles, neuronal loss, inflammatory processes), and 2) Loss of cholinergic neurons (and acetylcholine depletion) in the nucleus basalis of Meynert, which sends cholinergic projections to all areas of the neocortex, especially the temporal lobes and frontal and parietal association areas. The indemnity of this system is essential for normal cognitive functioning. At this moment, the only long term treatment available for AD are acetylcholinesterase inhibitors (CEIs) (e.g., tacrine, donepezil, rivastigmine, galanthamine). There are being investigated several treatments that may alter the development of neurofibrillary tangles and neuritic plaques (e.g., peripherally administered antibodies against beta amyloid proteins). Nerve growth factors may have the capability of improving neuronal survival, although their form of administration remains a problem. Amelioration of oxidative stress and CNS inflammatory processes may slow dawn the rate of neurodegeneration., Conclusion: All suspected mechanisms of the metabolic cascade of AD have been explored with specific and non specific treatments. Current treatments (e.g., CEIs) still have to prove that their effects can last for long periods of time. With the advent of further understanding of the neurodegenerative processes that cause AD, new treatments that may slow down the progression of the disease will be available.

Introduction and Development: Although the loss of episodic memory is considered one of the the hallmarks of Alzheimer s disease (AD), it is by no means the only memory dysfunction suffered by these patients. Perhaps equally important in terms of functional adaptation is the loss of, what Tulving referred, semantic memory. Semantic memory is that information necessary for language, a mental diccionary including not only lexical information (i.e., word meaning and concepts) but also facts and general world knowledge. There is a debate in the field of cognitive psychology regarding semantic memory, deficits in AD; whether there is an actual defect in semantic memory, or this is related to a disruption of the information accessing process. Neuroimaging studies have shown that the basis of the semantic memory defect is localized in the temporal and frontal lobes., Conclusions: The inferior temporal lobe, and perhaps more importantly, the parahippocampal gyrus, is critical for the ability to successfully name objects. However, the ability to retrieve name of objects appears to be associated with the frontal lobes.

Creutzfeldt-Jakob disease (CJD) is characterized by a rapidly progressive dementia that often leads to death within a few months of onset. However, some cases evolve over a much longer period of time and have a clinical picture that is difficult to distinguish from other progressive dementias that occur in the adult, especially Alzheimer's disease (AD). We examine the clinical features of 3 patients with pathologically confirmed CJD whose course was slow (4-5 years) and who were initially diagnosed as having AD. Only two of them had shown signs of CJD in the terminal stages. In this study we examine the clinical characteristics of these patients, and discuss of differentiating CJD from other entities, especially from AD.