Premium
Asymptomatic AD is associated with hypertrophy of CA1‐hippocampus neurons in the NUN study
Author(s) -
Iacono Diego,
Pletnikova Olga,
Rudow Gay,
Patel Ela,
Tudor Dianna,
Markesbery William,
Snowdon David,
Troncoso Juan C
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.707.2
Subject(s) - stereology , pathology , hippocampus , hippocampal formation , autopsy , asymptomatic , alzheimer's disease , nucleolus , disease , atrophy , medicine , neuroscience , dementia , muscle hypertrophy , psychology , nucleus
Objective: a) to measure differences in the volume of CA1 hippocampal neurons, and their nuclei and nucleoli in four different groups: subjects with Alzheimer's Disease (AD) pathology and no cognitive deficits (ASYMAD), mild cognitive impairment (MCI), definite AD (AD) and age‐matched controls (C). Introduction: the pathology of AD evolves decades before the disease becomes clinically manifest. Consequently, it is common to find substantial amounts of Aβ ‐plaques (NP) and neurofibrillary tangles (NFT) in autopsy brains of older subjects with normal cognition briefly before death (ASYMAD). Methods: we used designed‐based stereology to measure the volume of neuronal cell bodies, nuclei, and nucleoli in CA1. We examined postmortem brains of 13 C, 10 ASYMAD, 5 MCI, 10 AD subjects from the NUN study. Results: We found a significant hypertrophy of the neuronal cell bodies, nuclei, and nucleoli in CA1 of ASYMAD subjects compared to controls (p<0.01) and MCI (p<0.01). The hypertrophy of CA1 neurons in ASYMAD may represent a very early pathologic effect of A‐beta and tau on neurons or a reflection of cellular mechanisms that prevent the progression of the disease into dementia. Studies of the correlation of ApoE genotypes and ASYMAD are in progress.