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The Story Of Alzheimer’s Disease And CAV1

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Alzheimer’s Disease (AD) is amongst the main causes of morbidity and perhaps mortality in the older population1. Alzheimer’s disease pathology has over the years bordered on the deposition of the protein beta- amyloids (Aβ) and the subsequent involvement of tau plaques in the brains of patients. However, there has been evidence to suggest the involvement of vascular and endothelial factors 2 but this association is not clear. Writing in the journal of neuroscience, Bonds et al report that the reduction of Caveolin-1 (CAV-1) in a Type 2 diabetes (DM2) model induces the precursors of AD Pathology 3.

AD usually affects people in their mid-60’s and gradually progresses through life. Typical AD pathology reveals the increased presence of Aβ deposits and tau resulting in the death of brain cells. Typical symptoms include short-term memory loss and cognitive decline4. DM2 is characterized by a rise in blood sugar level due to insulin resistance or the bodies inability to produce properly functioning insulin5. Roberts and colleagues, DM2 significantly increased the risk of developing AD6. CAV-1 is mostly found in endothelial and fat tissues and helps in the trafficking of insulin via the blood-brain barrier into neural tissues7. It interacts with proteins within the lipid rafts and this is interesting since Amyloid Precursor Protein (APP) and BACE-1 processing also occur in the lipid raft8,9. This association with AD is a novel finding and opens a door into understanding the microvascular association.

The authors studied CAV-1’s role in AD. They checked the levels of CAV-1 in the brains of DM2 human patients and their controls and diabetic model mice also with their control group. Results showed significantly reduced CAV-1 levels in both human and mice T2D groups but not in both controls groups. Moving on, the reduced CAV-1 levels coincided with an increased level in APP, BACE-1 and Aβ in both diseased groups but was normal in the controls. Moving on, after CAV-1 reduction, irregularities in tau metabolism was assessed only in db/db mice. Results showed a significant increase in total tau which may have affected the AT8/DA9 ratio (fig 1)3.

With an Alzheimer’s disease model in place, the authors then sought to find out if there was any compromise to the functioning of the hippocampus. This was done by introducing novel and familiar test objects to see if they could remember. Unfortunately, diseased mice had difficulties in identifying the objects but when CAV-1 levels were increased, their performance levels increased significantly3. This meant CAV-1 reduction potentially affected the learning and memory performance of these mice.

Did CAV-1 reduction lead to AD pathology? To answer this question, the CAV-1 levels were increased in the diseased mice which resulted in a significant decrease in BACE-1, APP and tau levels in the brains of these animals. Further testing was carried out to determine if CAV-1 regulates the amyloidogenic pathway. Results showed significantly increased levels of Fl-APP, APP carboxyl-terminal fragments and Aβ when CAV-1 was underexpressed3. More importantly, this CAV-1 reduction resulted in a significant increase in human Aβ but not mice Aβ levels. When

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Taking their results together, Bond and colleagues were able to somewhat establish a link between T2D and AD however a few questions linger around their methods and some of their findings.

One inadequacy in this study is the fact that human Aβ cannot be found in the type of mouse strain (db/db) used. Thus, it makes it difficult to fully compare both parties since the expression of AD pathology in humans will be different from these mice. But the question remains, is there any other diabetic mouse strain that harbours human Aβ? Certainly not. Till another mice strain is found, it will be much appreciated if human organoids can be made from stem cells from AD individuals as this will certainly harbour the human Aβ and create a brain microenvironment that can be used to better understand the disease pathology. Also, this organoid model will afford the opportunity to easily manipulate genes and other proteins all in a bid to develop therapies to overcome the debilitating effects this condition comes with.

Secondly, the author’s use of the word depletion/ reduction was misleading. This is important because we do not know by how much CAV-1 was reduced. Was it by two folds, 30% or even 80%? Knowing to what level CAV-1 was depleted to or by how much will help in determining a threshold for future studies. This will help in the creation of a protocol and help in repeatability of these results. Lastly, the diseased test subjects used were all-male db/db mice and it is not clear why the author did not use female mice also or perhaps only female mice since it is known that there is not a statistical difference in gender relating to this strain of mice10.

In a paper by Chang et al, deletion of CAV-1 in an intracerebral haemorrhage (ICH) model resulted in a reduced brain injury11. This is different from the findings in this study which shows CAV-1 reduction rather increasing the AD pathology. The diseases might be different but shows that there might be a lot more happening behind the scene.

All in all, this paper certainly provides evidence for how these vascular and endothelial factors might induce AD pathology through DM2. Nevertheless, more work will need to be done to come up with a robust theory.


  1. Qiu, C., Kivipelto, M. and von Strauss, E., 2009. Epidemiology of Alzheimer’s disease: occurrence, determinants, and strategies toward intervention. Dialogues in clinical neuroscience, 11(2), p.111.
  2. Sweeney, M.D., Montagne, A., Sagare, A.P., Nation, D.A., Schneider, L.S., Chui, H.C., Harrington, M.G., Pa, J., Law, M., Wang, D.J. and Jacobs, R.E., 2019. Vascular dysfunction—The disregarded partner of Alzheimer’s disease. Alzheimer’s & Dementia, 15(1), pp.158-167.
  3. Bonds, J.A., Shetti, A., Bheri, A., Chen, Z., Disouky, A., Tai, L., Mao, M., Head, B.P., Bonini, M.G., Haus, J.M. and Minshall, R.D., 2019. Depletion of Caveolin-1 in Type 2 Diabetes Model Induces Alzheimer’s Disease Pathology Precursors. Journal of Neuroscience, 39(43), pp.8576-8583.
  4. Jack Jr, C.R., Bennett, D.A., Blennow, K., Carrillo, M.C., Dunn, B., Haeberlein, S.B., Holtzman, D.M., Jagust, W., Jessen, F., Karlawish, J. and Liu, E., 2018. NIA‐AA research framework: toward a biological definition of Alzheimer’s disease. Alzheimer’s & Dementia, 14(4), pp.535-562.
  5. Xu, W., Qiu, C., Winblad, B. and Fratiglioni, L., 2007. The effect of borderline diabetes on the risk of dementia and Alzheimer’s disease. Clinical Diabetology, 8(5), pp.188-195.
  6. Roberts, R.O., Geda, Y.E., Knopman, D.S., Christianson, T.J., Pankratz, V.S., Boeve, B.F., Vella, A., Rocca, W.A. and Petersen, R.C., 2008. Association of duration and severity of diabetes mellitus with mild cognitive impairment. Archives of neurology, 65(8), pp.1066-1073.
  7. Fridolfsson, H.N., Roth, D.M., Insel, P.A. and Patel, H.H., 2014. Regulation of intracellular signaling and function by caveolin. The FASEB Journal, 28(9), pp.3823-3831.
  8. Okamoto, T., Schlegel, A., Scherer, P.E. and Lisanti, M.P., 1998. Caveolins, a family of scaffolding proteins for organizing “preassembled signaling complexes” at the plasma membrane. Journal of Biological Chemistry, 273(10), pp.5419-5422.
  9. Vetrivel, K.S., Cheng, H., Lin, W., Sakurai, T., Li, T., Nukina, N., Wong, P.C., Xu, H. and Thinakaran, G., 2004. Association of γ-secretase with lipid rafts in post-Golgi and endosome membranes. Journal of Biological Chemistry, 279(43), pp.44945-44954.
  10. Ma, Y., Li, W., Yazdizadeh Shotorbani, P., Dubansky, B.H., Huang, L., Chaudhari, S., Wu, P., Wang, L.A., Ryou, M.G., Zhou, Z. and Ma, R., 2019. Comparison of diabetic nephropathy between male and female eNOS−/− db/db mice. American Journal of Physiology-Renal Physiology, 316(5), pp.F889-F897.
  11. Chang, C.F., Chen, S.F., Lee, T.S., Lee, H.F., Chen, S.F. and Shyue, S.K., 2011. Caveolin-1 deletion reduces early brain injury after experimental intracerebral hemorrhage. The American journal of pathology, 178(4), pp.1749-1761.

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