![]() In just 20 years, this number will likely double. The data supported previous findings from a study investigating neuropathologic and biochemical.Over 50 million humans suffer from dementia today. Oligomeric assemblies of soluble A pools were not different, but insoluble A - particularly A in formic acid and guanidine hydrochloride extracts - better distinguished pathological aging from AD. A42 levels, however, have been found elevated in pathological aging compared with AD, which probably represents greater abundance of diffuse plaques in pathological aging. Subtle quantitative differences were noted, but evidence from mass spectrometry identified more amino-terminal truncations in A of AD compared with pathological aging. Biochemical analyses of A peptides in pathological aging and AD revealed overlapping profiles. Moreover, A deposits in pathological aging had less codeposition of apolipoprotein E and the individuals had less advanced glycation end product immunoreactivity. Diffuse plaques, principally composed of A42, were more abundant in pathological aging, and paired helical filament tau immunoreactivity or glial reaction was rarely observed in proximity to senile plaques. ![]() Early investigations of pathological aging revealed that although senile plaque density was sufficient for AD according to Khachaturian criteria, morphologic and immunohistochemical differences existed between A deposits in pathological aging and AD. Some of the strongest data that support the hypothesis of a resistance factor in pathological aging come from neuropathologic and biochemical studies. This debate will briefly review the evidence for and against the notion that pathological aging is a state of resilience from the putative toxic effects of A.Įvidence supporting a resistance to amyloid-beta in pathological aging While increasingly recognized, there is a range of terms for pathological aging that makes review of the literature challenging, including presymptomatic or incipient AD, preclinical AD, pathological AD, nondemented high pathology controls, asymptomatic persons with AD neuropathology, intermediate probability mismatches, and pathologically preclinical AD. Recently, it was suggested that such individuals may have protective or resistance factors against the neuronal and synaptic pathology, which are structural correlates with cognitive impairment. Without longitudinal biomarker evidence to ascertain the timing of amyloid deposition, it is uncertain how long amyloid deposits have been present in the brains of individuals with pathological aging. Whether it is preclinical AD is controversial. Pathological aging is usually a finding in older individuals who have no significant antemortem cognitive impairment, and some individuals may even be high functioning. In pathological aging, however, significant A deposits (sufficient for a neuropathologic diagnosis of AD using Khachaturian criteria ) are detected in the setting of minimal cortical and limbic neurofibrillary pathology. In AD these lesions are accompanied by dendritic and synaptic abnormalities, as well as neuronal loss. The neuropathologic characteristics of pathological aging are extracellular amyloid-beta (A) in senile plaques and intracellular tau in neurofibrillary tangles and neuropil threads. Histopathologic changes characteristic of Alzheimer's disease (AD) have been described in nondemented older individuals, with particular focus on a form of senile cerebral amyloidosis - termed pathological aging. Author(s): Melissa E Murray 1 and Dennis W Dickson 1
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