Volume 31, Issue 1

Little is still known about the neuroanatomical substrates related to changes in specific cognitive abilities in the course of healthy aging, and the existing evidence is predominantly based on cross-sectional studies. However, to understand the intricate dynamics between developmental changes in brain structure and changes in cognitive ability, longitudinal studies are needed. In the present article, we review the current longitudinal evidence on correlated changes between magnetic resonance imaging-derived measures of brain structure (e.g. gray matter/white matter volume, cortical thickness), and laboratory-based measures of fluid cognitive ability (e.g. intelligence, memory, processing speed) in healthy older adults. To theoretically embed the discussion, we refer to the revised Scaffolding Theory of Aging and Cognition. We found 31 eligible articles, with sample sizes ranging from n = 25 to n = 731 (median n = 104), and participant age ranging from 19 to 103. Several of these studies report positive correlated changes for specific regions and specific cognitive abilities (e.g. between structures of the medial temporal lobe and episodic memory). However, the number of studies presenting converging evidence is small, and the large methodological variability between studies precludes general conclusions. Methodological and theoretical limitations are discussed. Clearly, more empirical evidence is needed to advance the field. Therefore, we provide guidance for future researchers by presenting ideas to stimulate theory and methods for development.

Crack cocaine is the crystal form of cocaine and can be smoked, and rapidly absorbed, and, in part for this reason, is potently addictive. It is hypothesized that crack cocaine is able to induce important changes in different tissues and organs, and thus dramatically alter behavior. Nevertheless, which alterations in the central nervous system are related to its frequent use is still a matter of discussion. The present study is a literature review of articles published between the years 2008 and 2018 on the theme ‘crack cocaine and brain’ available in PUBMED, MEDLINE, EMBASE, and Google scholar databases. The results show that the use of crack cocaine induces important behavioral, neuroanatomical, and biochemical alterations. The main behavioral sequelae include cognitive and emotional changes, such as increased anxiety and depressive symptoms, attention and memory deficits, and hyperactivity. Among the neurobiological alterations are reductions in the activity of the prefrontal, anterior cingulate cortex, and nucleus accumbens. Molecular changes include decreases in neurotrophic factors and increases in oxidative stress and inflammatory cytokines, which may be responsible for the morphological alterations observed. It is also hypothesized that these neurobiological changes might explain the emotional and cognitive dysfunctions experienced by crack cocaine addicts.

Alzheimer’s disease (AD) is a chronic neurodegenerative disease that locks into long clinical latency and low curative ratio. Therefore, early diagnosis before the clinical phase is quite essential and may be effective for therapeutic prevention. Peripheral blood or cerebrospinal fluid biomarkers symbolizing functional neuronal impairment are gradually applied to diagnose AD in research studies. Exosomes have generated immense interest in the diagnosis field of neurodegenerative disorders after confirmation of their roles as mediators, delivering important proteins and microRNAs (miRNAs) in intercellular communication. Compelling research results reveal that miRNAs released from exosomes modulate expression and function of amyloid precursor proteins and tau proteins. These findings open up possibility that dysfunctional exosomal miRNAs may influence AD progression. In this review, we summarized the existing knowledge of exosomal miRNAs and their involvement in AD, emphasizing their potential to serve as diagnostic biomarkers during the preclinical phase of AD.

Perineuronal oligodendrocytes (pn-Ols) are located in the cerebral gray matter in close proximity to neuronal perikarya and less frequently near dendrites and neurites. Although their morphology is indistinguishable from that of other oligodendrocytes, it is not known if pn-Ols have a similar or different cell signature from that of typical myelinating oligodendroglial cells. In this review, we discussed the potential roles of these cells in myelination under normal and pathophysiologic conditions as functional and nutritional supporters of neurons, as restrainers of neuronal firing, and as possible players in glutamate-glutamine homeostasis. We also highlighted the occurrences in which perineuronal oligodendroglia are altered, such as in experimental demyelination, multiple sclerosis, cerebral ischemia, epilepsy, Alzheimer’s disease, schizophrenia, major depression, and bipolar disorder.

Spikelets are small spike-like depolarizations that are found in somatic recordings of many neuron types. Spikelets have been assigned important functions, ranging from neuronal synchronization to the regulation of synaptic plasticity, which are specific to the particular mechanism of spikelet generation. As spikelets reflect spiking activity in neuronal compartments that are electrotonically distinct from the soma, four modes of spikelet generation can be envisaged: (1) dendritic spikes or (2) axonal action potentials occurring in a single cell as well as action potentials transmitted via (3) gap junctions or (4) ephaptic coupling in pairs of neurons. In one of the best studied neuron type, cortical pyramidal neurons, the origins and functions of spikelets are still unresolved; all four potential mechanisms have been proposed, but the experimental evidence remains ambiguous. Here we attempt to reconcile the scattered experimental findings in a coherent theoretical framework. We review in detail the various mechanisms that can give rise to spikelets. For each mechanism, we present the biophysical underpinnings as well as the resulting properties of spikelets and compare these predictions to experimental data from pyramidal neurons. We also discuss the functional implications of each mechanism. On the example of pyramidal neurons, we illustrate that several independent spikelet-generating mechanisms fulfilling vastly different functions might be operating in a single cell.