Neuroscientific Basis of Dementia


Product Description
In step with our growing lifespan, dementia is becoming a widespreadhandicap to the health and well-being of individuals and a burden on
human society world-wide. The increasing prevalence of this tragic
condition has stimulated an explosion of scientific research in the last
ten years, which resulted in numerous profound insights and technical
innovations. This timely volume presents both an overall and a detailed
overview of the current worldwide knowledge about the neuroscientific
basis of dementia.
Leading authorities in their fields provide a far-reaching synthesis of
all topics in dementia research, including pathogenesis of dementia,
neuroimaging of the earliest alterations, potential biological and
genetic markers for Alzheimer`s Disease and new therapeutic strategies.
Each chapter discusses clinical implications and areas of controversy,
highlights the wide range of current and future therapeutic
possibilities and indicates promising directions for further research...
Neuroscientific Basis of Dementia Review
Audience: Scientists and graduate students in medical, pharmacological and biological research, physicians and researchers in the biotechnological and pharmaceutical industries. Purpose: To give a comprehensive and detailed overview of the current worldwide knowledge about dementia disorders, particularly Alzheimer's disease (AD). Content: The book opens with two articles which deal with the phenomena of membrane lipid signaling, neuroinflammation and neuronal degeneration in AD. The next section, dealing with memory and its impairment, has chapters on long-term memory, amygdala damage in AD, memory in the hippocampus and hippocampal long-term potentiation. Then, there are eight chapters involving the tau protein that aggregates to cause neuronal degeneration in AD and other dementing disorders where neurofibrillary tangles and other tau deposits occur. These chapters include one on transgenic mice overexpressing the human tau who develop a progressive tauopathy similar to frontotemporal dementia with parkinsonism linked to chromosome 17, two on tau mutations, one which suggest that the amyotrophic lateral sclerosis/parkinsonism-dementia complex of the Kii peninsula is a new form of familial tauopathy, one on a new disease entity senile dementia of the neurofibrillary tangle type, and three on cellular pathology of tau. The next section contain three chapters on dementia related to synuclein. These papers show that alpha-synuclein is a common mediator of many neurodegenerative diseases, now called synucleinopathies (Parkinson's disease, dementia with Lewy bodies, LB variant of AD, multiple system atrophy) and give future directions for alpha-synuclein fibrillogenesis as target for drug development. The role of the presenilins (PS) in amyloid precursor protein (APP) processing and beta-amyloid (A-beta) production in AD is next covered in a series of thirteen chapters. These include seven on the presenilins and six on various aspects of beta-amyloid peptide. Cumulatively, these papers give evidence that the accumulation of A-beta peptide deposits (the presumed prime-mover in AD) in the cortex requires cleavage within the transmembrane domain of APP. Gamma-secretase has been posited as the agent responsible for this cleavage, but has managed to elude every effort to isolate and identify it. Four reports published in 1999 appear to be closing in on this long-sought goal. Three of them show that PS-1 is necessary for the cleavage of Notch, which mediates cell-cell interactions in determining cell fate during development. To carry out its signaling function, Notch requires cleavage in its transmembrane domain in a manner reminiscent of A-beta production. The fourth reports on mutations in PS-1 that completely abolish APP cleavage and suggests that PS-1 itself is gamma secretase (since two separate groups in Jan/Feb 2001 have found that transgenic mice lacking the BACE1 isoform of beta-secretase do not produce A-beta and grow to seemingly normal adulthood without unacceptable side-effects, now we know that a promising target for an AD therapy may be the beta-secretase as well). Finally, there are five chapters on the diagnosis and therapeutics of dementia. They comprise phenotype/genotype correlation in familial AD, risk factors and longitudinal studies of at-risk individuals from familial AD pedigrees, biological markers for differential diagnosis, cognitive deficits and functional neuroimaging techniques. One of these articles focused interest on the intake balance of polyunsaturated fatty acids called omega-3 and omega-6, which are not synthesized in mammals. The paper gives convincing evidence that genetic risk of AD might be lowered by the increased omega-6/omega-3 ratio (together with increased vitamin C, carotene and antioxidant levels). The last chapter gives a review of the recent progress of possible future therapeutic strategies. The most promising among these are anti-tau phosporylation (since recent demonstration that the propyl isomerase Pin-1 can restore the ability of phosphorylated tau to bind microtubules and promote microtubule assembly) and vaccine therapy (after a novel and exciting result of immunization of young monkeys, which produced high titres of serum A-beta antibody, almost completely prevented development of A-beta deposition, dystrophic neurites, astrocytosis and microgliosis, while immunization of the older animals also markedly reduced the extent and progression of the AD-like brain lesions). Highlights: The book is cohesive and highly readable. It fully covers a vast and scattered literature on latest progress in dementia research. Limitations: As with any multiauthored text, there is some redundancy. However, overlapping chapters on presenilins and A-beta are quite consistent with each other. Related reading: Two well-established books in the field are Alzheimer's disease and related disorders: Etiology, pathogenesis and therapeutics (Iqbal, Swaab, Winblad, Wisniewski, eds.; Wiley, 1999) and Alzheimer's disease (Terry, Katzman, Bick, eds.; Lippincot Williams & Wilkins, 1999). Before new editions of these books that are expected around 2003 or later, Neuroscientific basis of dementia neatly fits the gap and provide an integrative current view of one of the major medical problems of our time. Reviewer: Goran imi , MD, PhD, Department of Neuroscience, Crotian Institute for Brain Research, Zagreb University Medical School, Zagreb, Croatia.Most of the consumer Reviews tell that the "Neuroscientific Basis of Dementia" are high quality item. You can read each testimony from consumers to find out cons and pros from Neuroscientific Basis of Dementia ...

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