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The past decade has witnessed a revolution in the attempts of
scientists to under stand the molecular basis of dementia. Although
dementia, as defined by global cogni tive decline involving gradual
loss of memory, reasoning, judgment, and orientation, presents most
commonly in the form of Alzheimer's disease (AD), an assortment of
other less common disorders, such as prion and Pick's disease, can
also lead to symp toms that are similar to those observed in
patients with AD. The primary goal of Molecular Mechanisms of
Dementia is to address the various mechanisms and multi faceted
approaches currently being employed to more clearly delineate the
etiological and pathogenic events responsible for the onset of
dementia. Perhaps the greatest boon to obtaining a clearer
understanding of the causes of AD has come from genetic and
molecular biological studies carried out over the past decade. At
the genetic level, it has become increasingly clear that AD is a
heteroge neous disorder that can be broadly classified into two
categories. "Late onset" (>60 yr) cases, which account for the
vast majority of AD, genetically involve "susceptibility" genes
representing risk factors for the disease (e. g. , inheritance of
the 84 allele of the Apolipoprotein E gene). In many cases, the
susceptibility gene can act as a "modifier" that modulates the
pathogenic cascade occurring subsequent to a separate etiological
event "initiating" or "causing" the disorder.
The past decade has witnessed a revolution in the attempts of
scientists to under stand the molecular basis of dementia. Although
dementia, as defined by global cogni tive decline involving gradual
loss of memory, reasoning, judgment, and orientation, presents most
commonly in the form of Alzheimer's disease (AD), an assortment of
other less common disorders, such as prion and Pick's disease, can
also lead to symp toms that are similar to those observed in
patients with AD. The primary goal of Molecular Mechanisms of
Dementia is to address the various mechanisms and multi faceted
approaches currently being employed to more clearly delineate the
etiological and pathogenic events responsible for the onset of
dementia. Perhaps the greatest boon to obtaining a clearer
understanding of the causes of AD has come from genetic and
molecular biological studies carried out over the past decade. At
the genetic level, it has become increasingly clear that AD is a
heteroge neous disorder that can be broadly classified into two
categories. "Late onset" (>60 yr) cases, which account for the
vast majority of AD, genetically involve "susceptibility" genes
representing risk factors for the disease (e. g. , inheritance of
the 84 allele of the Apolipoprotein E gene). In many cases, the
susceptibility gene can act as a "modifier" that modulates the
pathogenic cascade occurring subsequent to a separate etiological
event "initiating" or "causing" the disorder.
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