Abstract
Alzheimer disease (AD) is a neurodegenerative disorder with an uncertain pathogenesis. It is characterised by symptoms of memory impairment, executive dysfunction and visuospatial impairment. Management goals and interventions should be based on a solid alliance with the patient and family and on thorough psychiatric, neurological and general medical evaluations of the nature and cause of cognitive deficits and associated non-cognitive symptoms. There are currently three cholinesterase inhibitors and one N-methyl-D-aspartate (NMDA) antagonist indicated in the treatment of AD as monotherapy or in combination. Cholinesterase inhibitors remain the first-line therapy in patients with mild to moderate AD, which may stabilise the symptomatic cognitive and functional decline. Other pharmacotherapy options include the use of memantine which may be used by itself or in combination with cholinesterase inhibitors. These treatments are for symptomatic relief and are not disease modifying in preventing the progression of the disease.
Highlights
Alzheimer disease (AD) is a neurodegenerative disorder with a pathogenesis and causes that are uncertain.[1]
Various other genes and proteins have been implicated in the pathogenesis of AD but that is beyond the scope of this review
Cerebrovascular disease is associated with worse cognitive performance in patients with AD and studies have suggested that cerebrovascular disease lowers the threshold for clinical dementia in patients with a diagnosis of AD.[41,42,43,44,45,46]
Summary
Alzheimer disease (AD) is a neurodegenerative disorder with a pathogenesis and causes that are uncertain.[1]. 5. Immunoreactive inclusions of transactive response DNA binding protein 43 kD (TDP-43) are commonly observed in cases with AD neuropathological change[16] www.tandfonline.com/oemd 28 The page number in the footer is not for bibliographic referencing helical filament (PHF) tau. Immunoreactive inclusions of transactive response DNA binding protein 43 kD (TDP-43) are commonly observed in cases with AD neuropathological change[16] www.tandfonline.com/oemd 28 The page number in the footer is not for bibliographic referencing helical filament (PHF) tau These are a major component of neurofibrillary tangles within the neuronal cytoplasm. Pathological forms of tau between neurons have been proposed as a mechanism by which AD spreads in the brain.[18,19,20] Various other genes and proteins have been implicated in the pathogenesis of AD but that is beyond the scope of this review. One must be aware that hypertension is a risk factor for cerebrovascular disease.[21,38,39,40] Cerebrovascular disease is associated with worse cognitive performance in patients with AD and studies have suggested that cerebrovascular disease lowers the threshold for clinical dementia in patients with a diagnosis of AD.[41,42,43,44,45,46]
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