Title of article :
Senile Dementia and Glaucoma: Evidence for a Common Link
Author/Authors :
Jain، Sachin نويسنده , , Aref، Ahmad A نويسنده ,
Issue Information :
فصلنامه با شماره پیاپی سال 2015
Pages :
7
From page :
178
To page :
184
Abstract :
Dementia and glaucoma are both neurodegenerative conditions characterized by neuronal loss leading to cognitive and visual dysfunction, respectively. A variety of evidence exists linking the two diseases including structural signs, specifically degenerative changes within ganglion cells. Both diseases become more prevalent with increased age, but that alone is unlikely to account for the increased co‑prevalence of the diseases found in various studies. Neurotoxic substances including abnormal hyperphosphorylated tau and amyloid‑β have been found in both disease processes suggesting possible pathophysiologic links between the diseases. The exact mechanism of apoptosis, whether by direct toxicity or potentiation, still needs to be established, but could prove important for both diseases. Another potential link relates to low intracranial pressure in patients with both diseases causing a high translaminar pressure gradient and optic nerve damage in certain patients. While this alone may not account for direct optic nerve damage, it could lead to cerebrospinal fluid (CSF) circulatory failure causing increased neurotoxins along the optic nerves with resultant damage. All of this evidence suggests the need to further study links between the two diseases, as this could prove instrumental in understanding their overlapping pathophysiology and developing directed therapies for both diseases. While this is more thoroughly investigated, it may be prudent to have a lower threshold for a glaucoma work‑up in patients with pre‑existing dementia.
Keywords :
Intraocular pressure , Optic nerve , Alzheimer dementia , Dementia , Glaucoma
Journal title :
Journal of Ophthalmic and Vision Research
Serial Year :
2015
Journal title :
Journal of Ophthalmic and Vision Research
Record number :
2403300
Link To Document :
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