A Blood-Based Biomarker May Be Able To Predict Alzheimer’s Disease

A Blood-Based Biomarker May Be Able To Predict Alzheimer’s Disease
A recent study describes a simple blood-based signature that reflects neocortical beta-amyloid burden.

Detecting Alzheimer’s disease by a relatively inexpensive blood test could greatly reduce the cost of population screening and recruitment for clinical trials. This is especially relevant given the hope that monoclonal antibodies directed at amyloid prove to modify the disease course.

 

A recent study published in Neurology, September 13, 2016, lead author Burnham, describes a simple blood-based signature that reflects neocortical beta-amyloid burden. It is a profile of 4 individual blood makers, specifically amyloid beta 1-42, CXCL-13, IgM-1, IL-17, PPY, and VCAM-1. Individually, they did not have significant predictive power but did in combination.

 

Specifically, the 12% of healthy controls that had high estimated beta-amyloid burden progressed in comparison to the 5% who had a low burden. Forty percent of subjects with mild cognitive impairment with a high burden progressed in comparison to 5% of those with MCI who did not. These ratios are similar to those utilizing Pittsburgh compound B-PET scan. They outperformed the cerebrospinal fluid amyloid-tau profile, which obviously requires an invasive lumbar puncture, as well as outperformed in measures of hippocampal volume on brain MRI. Keep in mind that there was marked overlap of confidence intervals in analyzing all of these markers.

 

If findings are confirmed in a large group of patients, this profile would likely come into widespread use. It appears that there are commercially available kits to measure each component.

 

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Race And Ethnicity In Multiple Sclerosis

Race and ethnicity are not the same. People of the same race share distinctive physical traits and ancestry. Ethnicity, on the other hand, is a shared experience, specifically cultural. DNA varies by less than 0.1% in any two people chosen at random. Further, at least 85% of the 350,000 known genes are present in all people.

 

African Americans in fact have higher incidence of MS than whites / Caucasians. Hispanic Americans seem to have lower incidence. People who migrate from a high risk to a low risk area in first two decades of life carry the high risk. This is more likely secondary to environmental factors, specifically vitamin D, and viral infections rather than genetic factors. Another important risk factor is obesity, especially in adolescent girls.

 

African Americans are older at onset and have a more severe course with resultant greater disability.

 

A Hispanic person can be of any race. In Hispanic Americans, age of onset appears to be younger than white but neuromyelitis optica much higher, with a prevalence of 19%, comparable to those in Asians. In whites, this disorder is seen in only 2% to 3%. Why should this be so? Likely, there is Asian ancestry in Hispanics from Central and South America.

 

Treatment of MS is greatly affected by race and ethnicity. African Americans are probably less responsive to interferons than whites. On the other hand, Tysabri may be effective in this group, as in Hispanic patients. B-cell therapies may be especially beneficial to African Americans because they have higher IgG index in their cerebrospinal fluid than whites. This, however, has never been tested adequately.

 

Access to healthcare is less in African Americans and Hispanics, especially low-income groups. About a third of patients in MS who are covered by Medicaid / Medi-Cal had never seen an MS specialist and were not receiving treatment-modifying drugs. Factors include mistrust of the healthcare delivery system (recall the Tuskegee syphilis study), less access to health insurance, greater belief in natural remedies, or as language and cultural barriers.

 

Tailoring treatment to a diverse group is a poorly met challenge at this time.

 

See Science of MS Management, summer 2016.

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What Anti-Epileptic Drugs Are FDA-Approved For Monotherapy?

FDA-Approved Anti-Epileptic Drugs  For Monotherapy
FDA-Approved Anti-Epileptic Drugs For Monotherapy

These are the FDA-Approved anti-epileptic drugs for monotherapy, the list is small:

 

  1. Felbamate for newly diagnosed and refractory focal.

 

  1. Lamotrigine for refractory focal and conversion to monotherapy.

 

  1. The next group consists of oxcarbazepine, topiramate, lacosamide, eslicarbazepine. These are all approved as monotherapy for newly diagnosed and refractory focal.

 

Note that levetiracetam is widely used as initial monotherapy for focal and generalized seizures although it is not FDA-approved for any monotherapy indication. This also holds for gabapentin, pregabalin, and zonisamide, although they are widely used as initial monotherapy.

 

Other than efficacy for a certain epilepsy syndrome, the type of adverse effects often guides choices. Drugs that may cause weight gain are valproic acid, gabapentin, pregabalin, carbamazepine, ezogabine, and perampanel. By contrast, topiramate, zonisamide, and felbamate may decrease weight. Lamotrigine and felbamate tend to be “alerting.” Pregabalin, lamotrigine, valproic acid, and carbamazepine may reduce anxiety. Zonisamide tends to be sedating. The sodium-channel blockers, such as carbamazepine and lacosamide, may cause imbalance and blurred vision. There are many other factors in choosing, such as enzyme induction and risks to the fetus. Those considered “safer in pregnancy” are levetiracetam, carbamazepine, oxcarbazepine, zonisamide, lamotrigine, and surprisingly phenytoin.

 

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