MEMORY : New Science to Improve Memory in Older Folks !

  Researchers at UC Irvine have discovered the ability to create lasting memories is linked to a newly discovered process: an enzyme blocking the release of of a gene called Period1 in the hippocampus of our brains. When we're young, turning this gene on is easy but as we get older this becomes harder.
  In each cell in our body there is 6 feet of DNA. As we age this spooled up length of DNA becomes less flexible (like our joints, eh?). This stiffness in our DNA is due to a "molecular brake pad" called HDAC3 that has become over-active in the aged brain and is compacting DNA too much and blocks the release of Period1.
  Removing the HDCA3 restores the flexibility and allows internal cell machinery to access Period1 to begin to form new memories.
  New drugs that target HDCA3 could allow older persons to improve memory formation ! 
  

Tumeric to Improve Memory

  From researchers at UCLA, daily oral curcumin (tumeric) may improve memory, mood and attention in cognitively normal middle-age and older adults. 
  Previous studies suggested that curcumin's anti-oxidant, anti-inflammatory, anti-amyloid and possible anti-tau properties may offer neuro-protective benefits. Prior human trials regarding the effects of circumin have been heretofore inconclusive.
  Doses tested of curcumin were 90 mg twice daily.
  GI side effects are possible such as abdominal pain and gastritis.
2017 Alzheimer's association International Conference

Hope for Alzheimer's Patients and Their Families ?

  As reported by Researchers Against Alzheimer's (RA2) there are 57 drugs in mid-stage testing (phase II) and 23 drugs in late-stage testing (phase III). These drugs could prevent or delay the symptoms of dementia. Phase II/III treatments include AC-1204, an oral drug for patients with mild to moderate Alzheimer's whose mechanism of action is to improve mitochondrial metabolism through chronic ketosis. Also, a combination of albumin and immunoglobulin administered IV with possible anti-amyloid antibodies and albumin binding capacity is in mid/late stage development to treat mild to moderate Alzheimer's disease.

Cummings J Alzheimers Res Ther. 2016;8;39

Caspase-2 a NEW potential Target in the Treatment of Alzheimer's

  Researchers at the University of Minnesota reported that capsase-2 , cuts the full length TAU protein (which accumulates in the brains of patients with AD and is neurotoxic) into fragments. These pieces of protein adversely affect synaptic signaling in dendritic spines directly leading to cognitive impairments in mice. These fragments PRECEDE the formation of aggregated TAU suggesting that the tangles seen are NOT the cause of AD. In fact the memory problems seen in these experimental mice occur BEFORE brain loss suggesting that blocking caspase-2 could be used to treat Alzheimer's disease.
Nat Med 2015:Epub 2016 Oct 10

PLIE Helps Patients with Alzheimer's

  PLIE (Preventing Loss of Independence Through Exercise) is a new program that combines elements of Eastern and Western traditional exercises and emphasizes focus on performing basic functional movements,encouraging social engagement and increasing bodily awareness. In the small group studied, patients would arrive at the exercise facility not remembering that they had been there but would start going through the movements of the routine. This fits with what we know about Alzheimer's : memory for events is impaired but procedural memory holds out and resists declination.
65th Annual AAN meeting San Diego March 2013
  In a related study, daily walking has been shown to stabilize Alzheimer's disease across one year.
Arch Gerontol Geriatr. 2013;56(1):96-103

Gene Mutation Increases Risk of Alzheimer's

  ABCA7 genetic mutation in African Americans nearly doubles the risk of Alzheimer's disease. It is not associated with the disease in Europeans.
JAMA April 10, 2013

Alzheimer's Disease Short Course Treatment

  This is a follow-up to a previous blog entry related to IVIG treatment of patients with Alzheimer's disease from the Mayo Clinic, Rochester,MN.
 Patients with early Alzheimer's disease receiving five doses of intravenous immunoglobulin (IVIG) over an eight week period  showed significantly less brain atrophy after 1 year than a placebo group.
  The problem is that IVIG is derived from human donor plasma and is extremely scarce supply. It's primary neurologic application to date has been in the treatment of patients with Guillain-Baré syndrome. Production capabilities for all current suppliers could not begin to provide enough for all patients with mild to moderate Alzheimer's disease, let alone the even larger population with mild cognitive impairment.
  Therefore, if a short-term dosing regimen is as effective as continuing therapy, it would extend current supplies that may be provided to a larger number of patients.

Kile S, et al "Initial findings of a randomized double-blinded placebo-controlled study of intravenous immunoglobulin in mild cognitive impairment due to Alzheimer disease" AAN 2013; Abstract P01.013.

Cotinine for Alzheimer's Treatment

A compound derived from tobacco, cotinine, reduced beta-amyloid plaque aggregation in the brain's of mice with the Alzheimer's disease model. The treated mice also performed better on tasks measuring working memory.
Journal of Alzheimer's Disease online Feb 14 2011