Elsevier

Brain Research

Volume 418, Issue 1, 18 August 1987, Pages 164-169
Brain Research

Loss of parvalbumin-immunoreactive neurones from cortex in Alzheimer-type dementia

https://doi.org/10.1016/0006-8993(87)90974-7Get rights and content

Abstract

The type and cell size of parvalbumin-immunoreactive (PV-Ir) neurones were examined in 14 postmortem brains from elderly control and Alzheimer-type dementia (ATD) patients with the aid of an image analyser. Morphological features of PV-Ir neurones suggested the existence of PV in the non-pyramidal interneurones in the cerebral cortex. A significant loss of PV-Ir cells was found in the frontal and temporal cortex in ATD. A significant reduction in the size of PV-Ir cells was also noted in the temporal cortex in ATD. These findings suggested that PV-Ir neurones in the cortex are affected in ATD.

References (33)

Cited by (106)

  • Pinpointing the locus of GABAergic vulnerability in Alzheimer's disease

    2023, Seminars in Cell and Developmental Biology
    Citation Excerpt :

    At the cellular level, numerous studies have characterised the relative vulnerability of GABAergic neurons in human AD brain (see Table 4). For example, early work in human post-mortem brain tissue from AD patients found evidence for reduced density and size of PV-positive interneurons in the frontal and temporal cortex [121]. However, this view was challenged by later findings reporting no change in the density of PV-positive neurons in AD-patient brain [122,123].

  • The interplay of neurovasculature and adult hippocampal neurogenesis

    2021, Neuroscience Letters
    Citation Excerpt :

    Moreover, it has been suggested that Aβ plaques can cause loss of hippocampal interneurons [37] and tau can accumulate in GABAergic interneurons [157], causing deficits in adult hippocampal neurogenesis. Interestingly, PVIs have been identified as one of the interneurons to be impaired in both human AD studies [6] and AD mouse models [43,45,79]. Neuronal loss [2,37], intrinsic electrical properties [79,139], hypersynchrony [100], and altered neural network activity [100,139] have been reported for PVIs in various regions of the brain.

  • Unsupervised excitation: GABAergic dysfunctions in Alzheimer's disease

    2019, Brain Research
    Citation Excerpt :

    Early studies found unaffected PV-positive neuron numbers in the temporal, visual and prefrontal cortex (Ferrer et al., 1991, 1993a; Hof et al., 1991; Leuba et al., 1998). Again, brain regions that are mainly affected by Aβ- and tau-pathology like the entorhinal cortex and hippocampus consistently showed decreased PV-positive neuron numbers (Arai et al., 1987; Brady and Mufson, 1997; Fonseca et al., 1993; Inaguma et al., 1992; Mikkonen et al., 1999; Satoh et al., 1991; Solodkin et al., 1996; Takahashi et al., 2010). Interestingly, impairments in neuronal network function like altered hippocampal oscillations have been shown to be associated with deficits in PV-positive inhibitory neuron function in AD and mouse models of AD (Verret et al., 2012); Chaper 2).

  • The dentate gyrus in Alzheimer's disease

    2007, Progress in Brain Research
    Citation Excerpt :

    The latter study is flawed by the fact that the total number of cases and immunoreactive cells is low. In other brain areas, a reduction is found, ranging between 20 and 72%, depending on brain region and layer (Arai et al., 1987; Solodkin et al., 1996; Mikkonen et al., 1999). Again, others differ when reporting no loss (Hof et al., 1991; Fonseca et al., 1993; Sampson et al., 1997; Leuba et al., 1998).

View all citing articles on Scopus

This work was supported by the research grant to H.A. from the Mental Health Foundation, U.K. and the Swiss National Science Foundation (3.147.0.85) to C.W.H.A. is a Visiting Research Fellow from the Psychiatric Research Institute of Tokyo, Tokyo 156, Japan.

View full text