Pathways towards and away from Alzheimer's disease

MP Mattson - Nature, 2004 - nature.com
Slowly but surely, Alzheimer's disease (AD) patients lose their memory and their cognitive
abilities, and even their personalities may change dramatically. These changes are due to …

How chronic inflammation can affect the brain and support the development of Alzheimer's disease in old age: the role of microglia and astrocytes

I Blasko, M Stampfer‐Kountchev, P Robatscher… - Aging cell, 2004 - Wiley Online Library
A huge amount of evidence has implicated amyloid beta (Aβ) peptides and other derivatives
of the amyloid precursor protein (βAPP) as central to the pathogenesis of Alzheimer's …

Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase

JL Jankowsky, DJ Fadale, J Anderson… - Human molecular …, 2004 - academic.oup.com
Amyloid precursor protein (APP) is endoproteolytically processed by BACE1 and γ-
secretase to release amyloid peptides (Aβ40 and 42) that aggregate to form senile plaques …

[HTML][HTML] Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration

CA Saura, SY Choi, V Beglopoulos, S Malkani… - Neuron, 2004 - cell.com
Mutations in presenilins are the major cause of familial Alzheimer's disease, but the
pathogenic mechanism by which presenilin mutations cause memory loss and …

[HTML][HTML] BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer's disease

M Ohno, EA Sametsky, LH Younkin, H Oakley… - Neuron, 2004 - cell.com
Abstract β-site APP cleaving enzyme 1 (BACE1) is the β-secretase enzyme required for
generating pathogenic β-amyloid (Aβ) peptides in Alzheimer's disease (AD). BACE1 …

Hippocampal long-term potentiation suppressed by increased inhibition in the Ts65Dn mouse, a genetic model of Down syndrome

AM Kleschevnikov, PV Belichenko… - Journal of …, 2004 - Soc Neuroscience
Although many genetic disorders are characterized by cognitive failure during development,
there is little insight into the neurobiological basis for the abnormalities. Down syndrome …

A focus on the synapse for neuroprotection in Alzheimer disease and other dementias

P Coleman, H Federoff, R Kurlan - Neurology, 2004 - AAN Enterprises
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD)
and are important targets for protective treatments to slow AD progression and preserve …

Amyloid-beta precursor protein processing in neurodegeneration

V Wilquet, B De Strooper - Current opinion in neurobiology, 2004 - Elsevier
The amyloid-β precursor protein is proteolytically cleaved by secretases, resulting in a series
of fragments, including the amyloid-β peptide of Alzheimer's disease. The amyloid precursor …

The role of insulin and insulin-like growth factor I in the molecular and cellular mechanisms underlying the pathology of Alzheimer's disease

E Carro, I Torres-Aleman - European journal of pharmacology, 2004 - Elsevier
Cellular and molecular processes leading to abnormal accumulation of β amyloid in the
brain are slowly being uncovered. A potential involvement of insulin and insulin-like growth …

β-Secretase inhibition for the treatment of Alzheimer's disease–promise and challenge

M Citron - Trends in pharmacological sciences, 2004 - cell.com
As the number of cases of Alzheimer's disease (AD) rises in all developed countries, the
unmet medical need for disease-modifying pharmacotherapy continues to grow. Much of AD …