**1. Introduction**

In the next lines, we do a brief journey through some aspects of gliomas, included epidemiological, clinical, neuroradiological, neuropathological, ultrastructural, therapeutics, and biologic behavior. An emphasis regarding the functional and therapeutics implications (metabolic therapy approach) of mitochondrial network (MN) and mitochondria-associated membranes (MAM) in astrocytomas is presented.

**3. Neuroimaging**

**4. Neuropathological aspects of gliomas**

**4.1. Gross pathology**

female patient with changes in behavior.

hemorrhage [11, 12].

**4.2. Histopathology**

Astrocytomas are most commonly seen on magnetic resonance imaging MRI as ill-defined, deep-seated, or predominantly subcortical cerebral hemispheric masses. MRI sequences, where signal hyperintensity reflects vasogenic edema generated in response to diffuse infiltration by individual tumor cells. Secondary signs of mass effect include midline shift, ventricular compression, and sulcal effacement. Glioblastoma commonly show a rim-enhancing pattern with a central low-density region of necrosis surrounded by irregular, variable thickness rim of contrast enhancement. This rim-enhancing component is always surrounded by T2- or FLAIR signal hyperintensity that represents an associated diffusely infiltrating neoplasm [11, 12] (**Figure 1**).

Functional and Therapeutic Implications of Mitochondrial Network and Mitochondria…

http://dx.doi.org/10.5772/intechopen.77224

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Diffuse astrocytomas are ill-defined and subtly discolored, with secondary mass effects. These tumors are most often centered in the subcortical white matter but have a tendency to infiltrate widely and include the cerebral cortex, deep gray structures, and even the contralateral hemisphere. Glioblastoma are classically heterogeneous, with foci of necrosis, and

**Figure 1.** Glioblastoma MRI. (A) Initial MRI from a 50-year-old male patient with seizures and a temporal lobe glioblastoma. (B) The same patient three months later. (C) A huge frontal lobe giant cell glioblastoma from a 65-years-old

Gliomas constitute a heterogeneous group of primary central nervous system tumors. The term astrocytoma includes tumors with astrocytic differentiation. They may have a wide spectrum of

The MN has been implicated in the process of carcinogenesis, which includes alterations of cellular metabolism and cell death pathways. Defects in mitochondrial function have been suspected to play an important role in the development and progression of cancer [1].

Accumulating evidence indicates that MAMs are a subcellular "hot spot" for the intracellular signaling [2, 3]. Recent research has highlighted and broadened the functional roles of MAM in a variety of cellular processes from lipid synthesis/transport, Ca2+ signaling, and ER stress, to mitochondrial shape and autophagy/mitophagy and to inflammation and cell immunity [3, 4]. MAM dysfunction has been associated with several types of cancer [5]. Research from the past decade has identified the MAM as a potentially central regulator of tumor cell metabolism, as exemplified by the presence of critical tumor suppressors and oncoproteins on this structure [6]. The involvement of MAM in cancer has not been thoroughly investigated. Consequently, there is a huge open window for pathophysiological understanding and novel treatment modalities related to MN and MAM functions.

Recently, we provide evidence showing MN and MAM ultrastructural aspects in a range of human astrocytomas, including pilocytic astrocytoma diffuse astrocytoma, anaplastic astrocytoma, and glioblastoma [7–10]. Probably, this represents a contribution to the structural basis of functional roles of MN and MAM in astrocytic tumors as well as therapeutics implications.
