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1.
Figure 1

Figure 1. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

Factors those are critical for healthy and extended lifespan in humans.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.
2.
Figure 5

Figure 5. Localization of mutant proteins of PD in the mitochondria in neurons affected by PD. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

In PD neurons, mutant proteins of α-synuclein, parkin, PINK1, and DJ1 are associated with mitochondria and cause mitochondrial dysfunction. Complex I activity is inhibited in PD neurons.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.
3.
Figure 4

Figure 4. The association of mutant huntingtin with mitochondria of HD neurons. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

In HD neurons, mutant Htt binds to outer mitochondrial membrane and induces free radical production, and may interrupt with calcium uptake. In HD, complex II of mitochondrial respiratory chain is affected.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.
4.
Figure 6

Figure 6. Localization of mutant proteins of SOD1 in the mitochondria in neurons affected by ALS. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

In ALS, mutant SOD1 is localized to inner, outer mitochondrial membranes, intermembrane space and matrix, and induce free radical production and oxidative damage. Impairment of Complex II and IV are associated with ALS.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.
5.
Figure 2

Figure 2. Structure of mitochondria. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

Mitochondria are bag like structures, comprised of 2 lipid membranes (outer and inner), and matrix that harbor components of tricarboxylic acid cycle, beta-oxidation. The electron transport chain is localized in the inner mitochondrial membrane. Outer mitochondrial membrane is porous, whereas mitochondrial inner membrane restricts ionic flow and protects the contents of matrix. Mitochondrial ATP is generated via oxidative phosphorylation within the inner mitochondrial membrane. Free radicals are generated as a byproduct of oxidative phosphorylation, primarily due to electron leaks in complex I and III of respiratory chain. The components of tricarboxylic acid, including α-ketoglutarate dehydrogenase, generate superoxide radicals in the matrix. These mitochondrially generated free radicals and superoxide radicals are carried to the cytoplasm via voltage-dependent anion channels and participate in lipid peroxidation, and protein and DNA oxidation.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.
6.
Figure 3

Figure 3. Localization of mutant proteins of AD in the mitochondria in neurons affected by AD. From: Mitochondria as a Therapeutic Target for Aging and Neurodegenerative Diseases.

In early-onset AD, genetic mutations of APP, PS1 and PS2 genes activate beta and gamma secretases, cleave from c-terminal region of amyloid beta precursor protein, and produce Aβ peptides. The toxic Aβ peptides enter mitochondria, interact with mitochondrial proteins, including cyclophilin D and ABAD --induce free radicals, decrease cytochrome oxidase activity, inhibit ATP generation and damage mitochondria both structurally and functionally. Further, in late-onset AD, APP is transported to outer mitochondrial membrane, blocks the import of nuclear cytochrome oxidase proteins to mitochondria and may be responsible for decreased cytochrome oxidase activity. In addition, N-terminal portion of ApoE4 is associated with mitochondria, induce free radicals and cause oxidative damage. In AD, complex IV of mitochondrial respiratory chain is affected.

P. Hemachandra Reddy, et al. Curr Alzheimer Res. ;8(4):393-409.

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