Dendritic Atrophy and Remodeling of Amygdaloid Neurons in Alzheimer's Disease

Abstract

The current study examined changes in the dendritic arbor of basolateral amygdaloid neurons in Alzheimer's disease (AD). Quantitative analysis of Golgi Kopsch-impregnated tissue samples revealed a significant reduction in the total dendritic length per neuron in AD. Terminal and nonterminal dendritic segments were affected similarly. Somatofugal ordering of the same segments, however, indicated that the reductions were restricted to the inner portion of the dendritic tree, coupled with significant AD-related increases in the length and number of the highest order segments. These data suggest that despite an overall AD-related loss of dendritic length in this amygdaloid subregion, new dendritic segments continue to form. The loss of proximal segments, combined with the gain of distal segments, may be interpreted as dendritic remodeling in the course of the disorder.

Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele

“…Chronic neuronal degeneration in a number of disorders related to quite different etiologies, such as AD, postalcoholic Korsakoff's disease, Parkinson's disease, or Huntington's chorea, is accompanied by growth and reorganization of the dendritic tree of certain types of neurons (Graveland et al, 1985;Arendt et al, 1986Arendt et al, , 1995bScott, 1993). These changes have been regarded as an attempt of the nervous system to counteract the functional impairments resulting from degenerative events.…”

Collapsin Response Mediator Protein-2: An Emerging Pathologic Feature and Therapeutic Target for Neurodisease Indications

“…AD is defined neuropathologically by the presence of both β-amyloid (Aβ) peptide-rich plaques and neurofibrillary tangles (NFTs, composed of abnormally phosphorylated microtubule-associated tau protein) in specific brain regions including the entorhinal cortex, hippocampus and isocortex; combined with loss of neural arborization and synaptic connections (i.e., frank neural atrophy) [30][31][32]. NFTs are located throughout the grey matter, but dystrophic neurites (axons) form in a distinctive corona about the plaques [30][31][32][33].…”

“…NFTs are located throughout the grey matter, but dystrophic neurites (axons) form in a distinctive corona about the plaques [30][31][32][33]. Although plaques and tangles are histologically dramatic, synapse loss is most consistently and significantly correlated to clinical dementia [30,34].…”

“…The most striking synaptic changes occur in close apposition with Aβ plaques where loss of dendritic spines (orthogonal presynaptic termini) is remarkable [35]. Loss of dendritic arborization in human AD also is well documented, for instance, manifesting as decreased average length per cell of Golgi-stainable branches and numbers of branches in particular amygdaloid and hippocampal neurons [31,32,34]. Although neuritic atrophy and synaptic structural pathology is subtler in AD mouse models than in human AD, synaptic deficits are inherent to the "triple transgenic mouse" [presenilin-1 (PS1)(M146V)KI; Thy1.2-amyloid precursor protein (APP)(swe); Thy1.2tau(P301L); "3xTg-AD"] that develops AD-like amyloid plaques and NFTs [36].…”

Alzheimer disease and neuroplasticity: New approaches and new targets in pharmacotherapy

“…Neocortex and hippocampus in AD also show massive somatodendritic sprouting (75,76), which may reflect unsuccessful remodeling in response to presynaptic or axonal damage (77). These dendritic changes therefore may be secondary to deafferation, signal transduction failures, or cytoskeletal abnormalities (15,73).…”