Alzheimer’s Group Resources

Losing a loved one in middle age can treble risk of developing dementia

MIDDLE-AGED people who live alone may have double the risk of developing dementia and Alzheimer's disease in later life compared with those who are married or living with (Source: Scotsman.com News - Health)

J&J Pays $1.5 Billion for Elan Stake

J&J will buy an 18.4% stake in Irish biotech company Elan, in a bid to crack the potentially lucrative Alzheimer's market. (Source: WSJ.com: Health)

Living Alone Increases Odds of Developing Dementia

Losing a partner through divorce or death in middle age may triple the risk, study shows Source: HealthDay Related MedlinePlus Topics: Alzheimer's Disease, Dementia, Seniors' Health (Source: MedlinePlus Health News)

Alzheimer’s disease summit: Translating research advances into clinical practice

The Alzheimer's Disease Summit, held on May 3, 2008, translated cutting-edge research into day-to-day practice. This supplement, based on information presented at the summit, presents valuable clinical content to a broad audience of primary care physicians, psychiatrists, geriatricians, and neurologists. (Source: Geriatrics Magazine)

Single Status at Middle-Age May Affect Alzheimer’s Risk

Middle-aged people who are widowed or divorced are more likely than their cohabiting counterparts to have cognitive impairment and Alzheimer's disease in later life, according to a study published online on July 2 in BMJ. (Source: Modern Medicine)

[Protein Structure and Folding] Insulin Receptor Dysfunction Impairs Cellular Clearance of Neurotoxic Oligomeric A{beta}

In this study we investigate whether impairments of insulin and insulin-like growth factor-1 (IGF-1) receptors play a role in aggregation of Aβ. Using primary neuronal culture and immortal cell line models, we show that expression of normal insulin or IGF-1 receptors confers cells with abilities to reduce exogenously applied Aβ oligomers (also known as ADDLs) to monomers. In contrast, transfection of malfunctioning human insulin receptor mutants, identified originally from patient with insulin resistance syndrome, or inhibition of insulin and IGF-1 receptors via pharmacological reagents increases ADDL levels by exacerbating their aggregation. In healthy cells, activation of insulin and IGF-1 receptor reduces the extracellular ADDLs applied to cells via seemingly the insulin-degra...

[Metabolism and Bioenergetics] Caspase-cleaved Tau Expression Induces Mitochondrial Dysfunction in Immortalized Cortical Neurons: IMPLICATIONS FOR THE PATHOGENESIS OF ALZHEIMER DISEASE

In this study we investigated the effects of T4C3 on mitochondrial function. Expression of T4C3 induced mitochondrial fragmentation and elevated oxidative stress levels in comparison with T4-expressing cells. Thapsigargin treatment of T4 or T4C3 cells, which causes an increase in intracellular calcium levels, resulted in a significant decrease in mitochondrial potential and loss of mitochondrial membrane integrity in T4C3 cells when compared with cells expressing T4. The mitochondrial fragmentation and mitochondrial membrane damage were ameliorated in T4C3 cells by pretreatment with cyclosporine A or FK506, implicating the calcium-dependent phosphatase calcineurin in these pathogenic events. Increased calcineurin activity has been reported in AD brain, and thus, inhibition of this phosphat...

J&J to Buy Elan Stake

J&J will buy an 18.4% stake in Irish biotech company Elan, in a $1.5 billion bid to crack the potentially lucrative Alzheimer's market. (Source: WSJ.com: Health)

J&J takes on Alzheimer’s disease with $1B stake in Elan

Johnson & Johnson, making a big jump into the risky but potentially lucrative field of Alzheimer's disease, is taking a major ... (Source: USATODAY.com Health)

Noggin and BMP4 co-modulate adult hippocampal neurogenesis in the APP(swe)/PS1(DeltaE9) transgenic mouse model of Alzheimer’s disease.

We report that decreased neurogenesis in the APP/PS1 transgenic mice was accompanied by increased expression of BMP4 and decreased expression of Noggin at both the mRNA and protein levels; statistical analysis showed that the number of proliferative cells at different ages correlated positively with Noggin expression and negatively with BMP4 expression. Intraventricular administration of a chimeric Noggin/Fc protein was used to block the action of endogenous BMP4; this resulted in a significant increase in the number of BrdU-labeled cells in dentate gyrus subgranular zone and hilus in APP/PS1 mice. These results suggest that BMP4 and Noggin co-modulate neurogenesis. PMID: 19463786 [PubMed - indexed for MEDLINE] (Source: Biochemical and Biophysical Research communications)