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P1‐213: Influence of history of traumatic brain injury on age at onset of cognitive impairment in MCI and Alzheimer's disease
Author(s) -
Li Wei,
Risacher Shan L.,
McAllister Thomas W.,
Saykin Andrew J.
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.413
Subject(s) - traumatic brain injury , medicine , alzheimer's disease neuroimaging initiative , apolipoprotein e , cognitive impairment , alzheimer's disease , psychology , disease , pediatrics , psychiatry
immunohistochemical stains. Frozen brain tissue was stored for DNA analysis. Results: The proband’s past medical history included hypertension, migraine headaches, and epilepsy during childhood. His mother died of a large stroke at 54 following 2 prior strokes, reportedly hemorrhages. Dementia was reported in a brother and a maternal uncle, both in their 60s. The proband’s mother and maternal niece had migraine headaches. Three months prior to death, the proband complained of intermittent headaches, dizziness, and balance difficulties. MRI revealed a left occipital subcortical hemorrhage and multiple small white matter lesions, suspicious for hemorrhages. Cerebral angiography revealed a deep tentorial-perithalamic arteriovenous malformation (AVM). Although the relationship to the occipital hemorrhage was unclear, stereotactic radiation therapy for the AVM was scheduled. Before therapy began, death occurred from a large left frontoparietal lobe cerebral hemorrhage. At autopsy, the 1480 gram brain showed diffuse swelling with intraparenchymal and subarachnoid hemorrhage. Histological and immunohistochemical studies confirmed the presence of b-amyloid through the full thickness of all sizes of leptomeningeal and cortical blood vessels and some white matter vasculature. Vessel-in-vessel appearance was noted. Frequent cortical b-amyloid plaques and tau-positive neurofibrillary tangles were present, indicative of AD. Sequencing of the b-Amyloid Precursor Protein gene is underway. Conclusions: Clinically, the pattern of multiple cerebral hemorrhages, including subcortical and lobar distribution on MRI, strongly suggested CAA. Based on the autopsy confirmation of severe and extensive CAA in the proband’s brain, along with age and family history, a hereditary b-amyloid disorder is possible and under evaluation. (Grants: P30 AG 35982, P30 AG 010133.)