Monday, 17 April 2017

Alzheimer’s Disease – Now You See It

The exact mechanisms underlying the devastation that is Alzheimer’s Disease (AD) are not entirely understood, but researchers do know that inflammation in the brain is related to the onset of the disease. Now, through a basic eye exam, clinicians may be able to spot AD warning signs, including inflammation, long before symptoms appear

Normally, the brain depends on tau protein to receive nutrients and get rid of waste. When a toxic form of the tau protein clumps together, it forms tangles that are noxious to the brain. These toxic tau proteins may be at least partly responsible for the inflammation that is characteristic of AD, and inflammation may start before the tau tangles form. Now, researchers at the University of Texas speculate that this inflammation may be detectable by examining the retina during routine eye exams. This type of screening would be non-invasive and inexpensive and may eventually allow for early intervention to mitigate brain cell death and cognitive decline.

Authors of the current study, published in Journal of Alzheimer’s Disease, examined brain analyses and retinal samples from human patients with AD, as well as a mouse model of AD. The findings suggest that toxic tau proteins induce inflammation that spreads throughout the brain, initiating the vicious cycle of cell death and more inflammation. Screening of the retina as part of a normal health check-up can detect inflamed tissue earlier in the disease process than other methods of AD screening.

AD has long been known to impact the visual system, and pathophysiological connections have been made between AD and visual disorders, such as certain types of cataract and glaucoma. The eye offers easy access to cerebral functioning, and ocular biomarkers for AD may potentially improve disease diagnosis and management.

AD is the most common form of dementia and its prevalence is growing as the world’s population ages. Patients with AD exhibit profound, progressive declines in cognition, memory, and social functioning. To date, there are no cures and available treatments are only marginally effective at managing some of the symptoms of the disease.

The new findings are far from offering cures or preventions for AD, but the authors hope that, eventually, early detection of inflammation will lead to therapeutic options for reducing inflammation and minimizing neurodegenerative brain damage.

References

Hart NJ, Koronyo Y, Black KL, Koronyo-Hamaoui M. Ocular indicators of Alzheimer’s: exploring disease in the retina. Acta Neuropathol. 2016;132(6):767-787. PMID: 27645291.

Javaid FZ, Brenton J, Guo L, Cordeiro MF. Visual and ocular manifestations of Alzheimer’s disease and their use as biomarkers for diagnosis and progression. Front Neurol. 2016;7:55. PMID: 27148157.

Jun G, Moncaster JA, Koutras C, et al. ?-Catenin is genetically and biologically associated with cortical cataract and future Alzheimer-related structural and functional brain changes. PLoS One. 2012;7(9):e43728. PMID: 22984439.

Kusne Y, Wolf AB, Townley K, et al. Visual system manifestation of Alzheimer’s disease. Acta Ophthalmol. 2016. PMID: 27864881.

Nilson AN, English KC, Gerson JE, et al. Tau oligomers associate with inflammation in the brain and retina of tauopathy mice and in neurodegenerative diseases. J Alzheimers Dis. 2016. PMID: 27716675.

Valenti DA. Alzheimer’s disease and glaucoma: imaging the biomarkers of neurodegenerative disease. Int J Alzheimers Dis. 2011. PMID: 21253485.

Image via cocoparisienne / Pixabay.

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